Sie sind auf Seite 1von 24

http://cre.sagepub.

com/
Clinical Rehabilitation
http://cre.sagepub.com/content/16/3/276
The online version of this article can be found at:

DOI: 10.1191/0269215502cr491oa
2002 16: 276 Clin Rehabil
Lynne Turner-Stokes and Diana Jackson
an integrated care pathway
Shoulder pain after stroke: a review of the evidence base to inform the development of

Published by:
http://www.sagepublications.com
can be found at: Clinical Rehabilitation Additional services and information for

http://cre.sagepub.com/cgi/alerts Email Alerts:

http://cre.sagepub.com/subscriptions Subscriptions:
http://www.sagepub.com/journalsReprints.nav Reprints:

http://www.sagepub.com/journalsPermissions.nav Permissions:

http://cre.sagepub.com/content/16/3/276.refs.html Citations:

What is This?

- Mar 1, 2002 Version of Record >>


at PENNSYLVANIA STATE UNIV on June 5, 2014 cre.sagepub.com Downloaded from at PENNSYLVANIA STATE UNIV on June 5, 2014 cre.sagepub.com Downloaded from
Clinical Rehabilitation 2002; 16: 276298
Arnold 2002 10.1191/0269215502cr491oa
Address for correspondence: Lynne Turner-Stokes, Regional
Rehabilitation Unit, Northwick Park Hospital, Watford
Road, Harrow, Middlesex HA1 3UJ, UK. e-mail:
lynne.turner-stokes@kcl.ac.uk
Shoulder pain after stroke: a review of the
evidence base to inform the development of
an integrated care pathway
Lynne Turner-Stokes and Diana Jackson Northwick Park and St Marks Hospital Trust, Harrow, Middlesex, UK
Received 3rd May 2000; returned for revisions 28th June 2000; revised manuscript accepted 16th October 2000.
Background: Shoulder pain is a common complication of stroke. It can
impede rehabilitation and has been associated with poorer outcomes and
prolonged hospital stay. This systematic review was undertaken to inform the
development of an evidence-based integrated care pathway (ICP) for the
management of hemiplegic shoulder pain (HSP).
Aims and objectives:
1) To provide a background understanding of the functional anatomy of the
shoulder and its changes following stroke.
2) To review the literature describing incidence and causation of HSP and the
evidence for factors contributing to its development.
3) To appraise the evidence for effectiveness of different interventions for
HSP.
Methods: Data sources comprised a computer-aided search of published
studies on shoulder pain in stroke or hemiplegia and references to literature
used in reviews (total references = 121).
Main ndings: Although a complex variety of physical changes are associated
with HSP, these broadly divide into accid and spastic presentations.
Management should vary accordingly; each presentation requiring different
approaches to handling, support and intervention. (1) In the accid stage, the
shoulder is prone to inferior subluxation and vulnerable to soft-tissue damage.
The arm should be supported at all times and functional electrical stimulation
may reduce subluxation and enhance return of muscle activity. (2) In the
spastic stage, movement is often severely limited. Relieving spasticity and
maintaining range requires expert handling; overhead exercise pulleys should
never be used. Local steroid injections should be avoided unless there is clear
evidence of an inammatory lesion.
Conclusions: HSP requires co-ordinated multidisciplinary management to
minimize interference with rehabilitation and optimize outcome. Further
research is needed to determine effective prophylaxis and document the
at PENNSYLVANIA STATE UNIV on June 5, 2014 cre.sagepub.com Downloaded from
Shoulder pain after stroke 277
Introduction
Shoulder pain is a common and distressing com-
plication of stroke, interfering with both function
and quality of life.
1
If the shoulder is very painful
the patient may prefer not to move, or may with-
draw from active rehabilitation.
2
A protected and
immobile shoulder may interfere not only with
upper limb function, but with balance, walking,
transfers and performance of self-care activities.
3
Hemiplegic shoulder pain (HSP) can therefore
impede the process of rehabilitation, and has
been associated with poorer outcomes and
increased length of stay in hospital.
4,5
To address this problem, hemiplegic shoulder
pain was selected as an appropriate area for
development of an integrated care pathway
(ICP). In keeping with the principle that the ICP
should be based on evidence, and as a prelimi-
nary step in its development, a systematic review
of the literature was undertaken. The authors
would like to stress that this review is not
intended to be a Cochrane style review around a
limited research question with clear exclusion cri-
teria, odds ratio calculation, etc. Instead we have
taken a systematic approach to searching the rel-
evant literature to assimilate current knowledge
and appraise the evidence for each aspect of clin-
ical management. The aims of the review were:
1. To provide the reader with a background
understanding of the functional anatomy of
the shoulder and how it is affected by stroke.
2. To review the literature describing frequency
and causation of HSP and the evidence for
factors contributing to its development, thus
indicating potential routes to prevention.
3. To appraise the evidence for effectiveness of
different interventions for HSP.
From this we have drawn conclusions on best
practice to underpin an ICP for the multidisci-
plinary management of HSP which is presented
separately for publication.
Search strategy
Electronic literature searches were performed
through the British Medical Association Ovid
Online service using the following keywords:
1) Shoulder pain or shoulder dislocation or
shoulder impingement syndrome or shoulder
injury or frozen shoulder
2) Stroke (all subheadings)
3) Hemiplegia or hemiplegic.mp
4) Hemiparesis or hemiparetic
5) 2 or 3 or 4
6) 1 and 5.
References from EMBASE 19882000 (n = 63)
and MEDLINE 19662000 (n = 44) were pooled
and duplicates discarded leaving 91 references. In
addition, relevant references listed in review arti-
cles,
1,613
but not identied in the search (usually
because they were journals or books that were
not indexed) were obtained, giving a total of 121
articles included in the review.
Functional anatomy of the shoulder
and changes following a stroke
In order to understand the literature, it is help-
ful to have a background understanding of the
functional anatomy of the shoulder and how this
may be changed by a stroke.
In humans, the shoulder has evolved to pro-
vide an extended range of movement in order to
facilitate hand placement for dextrous function.
However, this extended range is at the expense
of stability.
14
The shoulder is formed by a com-
plex system of ve articulations.
Glenohumeral joint (GHJ)
Subacromial bursa (SAB)
Acromioclavicular joint (ACJ)
Sternoclavicular joint (SCJ)
Rotation of the scapula on the thoracic wall.
The main glenohumeral joint is a ball-and-socket
joint with a relatively small area of bony contact
therapeutic effect of different modalities in the various presentations.
Development of an integrated care pathway provides a reasoned approach to
management of this complex condition, thus providing a sound basis for
prospective evaluation of different interventions in the future.
at PENNSYLVANIA STATE UNIV on June 5, 2014 cre.sagepub.com Downloaded from
278 L Turner-Stokes and D Jackson
2) Humeral rotation which alters the position of
the humeral tubercles in relation to the arch.
Flexion must be accompanied by medial rota-
tion (subscapularis) and abduction by lateral
rotation (infraspinatus) to avoid impinge-
ment.
18
Failure of any of these mechanisms to operate
during elevation of the arm will cause impinge-
ment of supraspinatus or the long head of
biceps.
19
Repeated episodes of mechanical wear
may result in a vicious cycle of pain, inamma-
tion and the risk of further damage to the cuff by
compression or ischaemia.
Changes with age
Since most strokes occur in the sixth or sev-
enth decade, it is pertinent to consider the nor-
mal changes that occur with age in the shoulder
structures, which are likely to represent normal-
ity in that age group. Painless range of movement
in the shoulder decreases with age
20
as a result of
postural change and degeneration in the articu-
lar surfaces and soft tissues around the complex
of joints.
21
The development of dorsal kyphosis
may further restrict the available range of shoul-
der elevation. Degenerative changes in the ACJ,
glenoid labrum, and articular cartilage of the gle-
noid fossa start to appear after the second decade
of life.
18
The rotator cuff thins and frays and cal-
cic deposits may appear in the tendons. Synovial
hypertrophy in the subacromial bursa and osteo-
phytic change in the ACJ serve to narrow the
subacromial space and increase the likelihood of
damage to the already weakened rotator cuff.
Partial tears of the rotator cuff are common after
the age of 5060 years, and the most severe tears
occur from 60 to 70 years.
18
Shoulder pain is rec-
ognized as a common problem among the gen-
eral population, with an estimated yearly
reported incidence of 12.5%
22,23
and with the
greatest proportion of shoulder problems being
reported during the 5th7th decades.
22
Changes following a stroke
Immediately following central motor lesions,
such as stroke, there is an initial accid paralysis
in over 90% of individuals
24
which is often
replaced by a predictable pattern of spasticity in
a timescale which may vary from 24 hours
24
to
1218 months
2527
Alteration in the alignment of
enlarged by the cartilaginous glenoid labrum
which enhances stability without restricting
movement.
15
The role of the rotator cuff muscles
is to tuck in the humeral head to form a stable
fulcrum for elevation.
16
An important function of
this tucking-in is that the humeral head is low-
ered away from the acromion. If rotator cuff
function is damaged by paralysis or degeneration,
the humeral head may ride up on the glenoid sur-
face.
17
This is a likely cause of impingement of
the supraspinatus tendon between the humeral
head and the acromion (Figure 1).
In addition to this tucking-in function, two
other mechanisms serve to minimize impinge-
ment and maintain stability during shoulder ex-
ion and abduction:
1) Upward rotation of the scapula which ele-
vates the coracoacromial arch and allows the
glenoid to maintain a position of rm oppo-
sition to the humeral head.
15
Scapular rota-
tion is principally controlled by the trapezius
and serratus anterior muscles.
15
Figure 1 Shoulder structures and impingement of the
supraspinatus tendon.
at PENNSYLVANIA STATE UNIV on June 5, 2014 cre.sagepub.com Downloaded from
Shoulder pain after stroke 279
skeletal components of the shoulder complex
have been described in both the accid and spas-
tic stages of paralysis after stroke, and each has
been implicated in the causation of HSP.
In accid paralysis of the shoulder, weakness
in the shoulder girdle muscles and gravitational
pull tend to result in inferior subluxation,
although the exact mechanism for this remains
the subject of debate.
2832
In addition, weakness
in the muscles that effect scapular and humeral
rotation during elevation results in failure of the
mechanisms that normally protect against
impingement. The danger of rotator cuff damage
during passive elevation of the arm is therefore
increased.
33
The weight of the unsupported arm
may also cause traction damage to various nerves
including the axillary nerve,
34
the suprascapular
nerve
35
and the brachial plexus.
36,37
Nerve dam-
age itself could then serve secondarily to com-
pound shoulder girdle weakness.
37
As spasticity develops, activity in the
supraspinatus muscles may reduce inferior sub-
luxation,
26
but now the scapular rotation may be
impeded by increased tone in the latissimus dorsi,
levator scapulae and rhomboid muscles.
29
Fur-
thermore, activity in the medial rotators may pull
the humerus into internal rotation, thus con-
tributing to impingement on active and passive
GHJ abduction. The humeral head may now be
anteriorly displaced. However, if inferior sublux-
ation was severe during the accid stage, it may
remain inferiorly displaced due to permanent
stretching or damage to the rotator cuff.
33,38
Increased muscle tone may cause pain by pro-
ducing sustained traction on periosteal muscle
attachments, which are rich in sensory receptors.
2
Such spasticity interferes with normal scapulo-
humeral movement and increases the likelihood
of contractures.
8
Once contractures have devel-
oped, attempts to stretch the contracture cause
pain, generating reex protective spasm and
patient apprehension. There is consequently a
vicious cycle of reduced movement, increasing
restriction with disuse atrophy and osteoporosis
occurring as late events.
29
In summary, it appears that deranged anatomy
in both accid and spastic stages may contribute
to HSP, although the mechanisms are different.
In the next section we review the evidence for
these mechanisms in greater detail. It will be seen
that the evidence is confounded by the fact that
many patients go through both stages and, unfor-
tunately, the relative incidence of spasticity and
accidity to HSP in the literature are not well
documented.
8
On top of either condition, soft-tis-
sue damage resulting from improper handling
presents a further confounding factor.
8,9,12
Incidence and causation of HSP and
the evidence for factors contributing
to its development
Reports of frequency of shoulder pain in the lit-
erature vary between 5 and 84% and are listed
in Table 1. There are a number of reasons for this
variation. Many of the studies are retrospective
and so must be regarded with caution. The g-
ures are also difcult to compare, as many of the
populations are selected and it is not always clear
whether incidence or prevalence is being
reported.
12
Most of the epidemiological data have
been gathered from patients attending rehabili-
tation programmes, so the incidence of HSP is
unknown in patients not attending for rehabilita-
tion, those with mild disability only, or those who
have been discharged from treatment.
9
Pain is not consistently described. Some stud-
ies appear to be reporting pain which occurs
spontaneously,
4,33,39,40
but some report only pain
on passive movement.
41,42
Others include either
type of pain
2,34,43
and only a few studies make a
clear distinction between them.
4447
If pain is cat-
egorized by severity, mild pain may be included
either with the no pain
48
or the some pain
41
category.
Pain is a subjective symptom which is difcult
to measure even in patients with intact sensori-
motor, cognitive and communication facilities.
Standard pain assessment techniques such as
visual analogue scales may be inappropriate for
patients with visuospatial neglect, and self-com-
pleted questionnaires, such as the McGill Pain
Score
49
may be inaccessible for patients with
aphasia. Price et al. have demonstrated that
stroke patients as a group form poor witnesses
for many types of visual analogue scale.
50
Bohnannon and Andrews used the Ritchie index
to measure shoulder pain in stroke patients
51
and
reliability testing suggests that agreement using
at PENNSYLVANIA STATE UNIV on June 5, 2014 cre.sagepub.com Downloaded from
280 L Turner-Stokes and D Jackson
demonstrated an association.
40,41,44
As will be shown later in this review, within
the group of patients with substantial upper limb
decits, it is likely that other factors such as soft
tissue damage or spasticity may intervene to have
a greater effect on pain, than severity of the
stroke decit per se.
Time after stroke is also a factor. As already
described, the natural progression of hemiplegia
over time is characterized by changes in muscle
tone, weakness and loss of normal range of
movement. All these have an effect on normal
shoulder posture and render the shoulder vul-
nerable to contractures and soft tissue damage
from inappropriate handling. It is not surprising,
therefore, to nd that the likelihood of develop-
ing HSP increases over time. Prospective studies
report HSP starting almost immediately after
stroke in a few patients, with the majority devel-
oping pain some weeks or months later.
4,46
In one
longitudinal study,
58
pain and stiffness were
found to be present in 16% of their 135 patients
at two weeks post stroke, but by one year an
additional 27% complained of pain. Bohannon et
al.
41
showed an inter-relationship between time
since stroke, range of shoulder external rotation
and severity of shoulder pain.
this method of rating is substantial.
42
Assess-
ments based on shoulder function
52
are unsuit-
able in the nonfunctional upper limb. There is as
yet no well-validated instrument specically
developed for dening shoulder pain in stroke
patients.
Most studies agree that HSP is independent of
age and sex.
9,44
Reports vary with regard to side
of stroke, and some have found no relationship
at all.
44
On the other hand, it has been postulated
that patients with neglect, due to right hemi-
sphere damage, may not protect their paralysed
upper limb effectively and therefore be at greater
risk of trauma. Poulin de Courval et al.
45
found
that pain was signicantly more common in left
hemiplegics, but there was no relationship
between pain and the presence of left hemi-
neglect. By contrast, other studies have found a
preponderance of right hemiplegia in association
with HSP.
53,54
Many authors concur that the incidence of pain
is related to severity of paresis.
4,55,56
In a group of
patients with severe paralysis,
33
84% of patients
had moderate or severe shoulder pain. Patients
with slight paresis only rarely complain of shoul-
der pain,
57
and the reference reporting the
lowest incidence of HSP was a community-based
study
47
in which 26% of patients had no arm
weakness. On the other hand, not all authors
Table 1 Reported rates of occurrence of shoulder pain
Author and year Number in series Incidence of HSP (%)
Najenson 1971
33
32 27 (84%)
Braun 1971
2
100 70 (70%)
Hurd 1974
88
14 8 (57%)
Brocklehurst 1978
58
107 73 (43%)
Tepperman 1984
43
85 17 (21%)
Van Oewenaller 1986
63
219 157 (72%)
Parker 1986
47
187 9 (5%)
Bohannon 1986
41
50 36 (72%)
Bohannon 1990
42
24 17 (70%)
Poulin de Courval 1990
45
94 45 (48%)
Ring 1993
56
80 43 (53%)
Roy 1994
4
76 55 (72%)
Cheng 1995
44
50 32 (64%)
Jesperson 1995
39
173 38 (22%)
Zorowitz 1996
40
20 9 (45%)
Wanklyn 1996
11
108 69 (64%)
Range = 584%
Mean = 54%
HSP, hemiplegic shoulder pain.
at PENNSYLVANIA STATE UNIV on June 5, 2014 cre.sagepub.com Downloaded from
Shoulder pain after stroke 281
resistance to passive stretch may result from
other factors, such as the viscoelastic properties
of soft tissues, and indeed, resistance to move-
ment may be more marked in the presence of
pain.
64
In addition, tone patterns can vary within
the same hemiplegic arm, such that there is ac-
cidity around the shoulder and spasticity distally,
or vice versa. They may also vary from day to
day.
4
None of the authors make a clear distinc-
tion between the presence of spasticity speci-
cally in the shoulder girdle muscles, as opposed
to more generally in the upper limb. A positive
association between pain and spasticity was
found in three studies.
38,45,63
Shahani et al.
38
reported an association between degree of pain
and degree of spasticity, but their study only
included 10 patients. In the much larger study by
Van Ouwellaner et al.
63
of 219 patients there was
a particularly strong association between pain
and spasticity: 85% of patients with spasticity
around the shoulder complained of pain, as com-
pared with only 18% of those with accidity.
Other authors have failed to nd a direct asso-
ciation between HSP and upper limb spasticity
Spasticity and accidity
Tobis
59
describes the typical picture of HSP as
accid paralysis, atrophic shoulder musculature
and inferior subluxation. However, Bobath
claims that shoulder pain only becomes a prob-
lem when spasticity develops.
60,61
Physiothera-
peutic reviews
9,12
in particular have drawn
attention to the role of spasticity in shoulder
pain, because of the different therapeutic strate-
gies employed to manage it.
62
Table 2 summa-
rizes the papers that describe the relationship
between HSP, spasticity and limitation of exter-
nal rotation.
Spasticity is dened as a velocity-dependent
resistance to passive stretch
1
but not many stud-
ies have specically separated spastic and accid
shoulder pain in their analysis, nor is there
agreement on how spasticity is assessed. Most
studies simply state that tone was
assessed,
41,44,48,56
but some authors assessed spas-
ticity on the basis of an increased myotatic
(stretch) reex,
63
and others used the Ashworth
scale.
4
Doubt has been cast on the Ashworth
scale as a valid measure of spasticity because
Table 2 Relationship between HSP, spasticity and limitation of external rotation
Author and year Number Spasticity Method for assessing spasticity HSP HSP related to
in series assessed related to reduced range of
spasticity external rotation
Van Ouwenaller 1986
63
219 Yes Myotatic reex Yes Not mentioned
Bohannon 1986
41
50 Yes Simultaneously with range during No Yes
external rotation
Poulin de Courval 94 Yes Physiotherapy assessment of Yes Yes
1990
45
muscle tone:
Flaccid = 0 Normal = 1
Spasticity: 2 = mild, 3 = moderate,
4 = severe
Joynt 1992
48
67 Yes Resistance to rapid stretch No Yes
Ring 1993
56
80 Yes Clinical assessment Trend, Not mentioned
Normal tone, hypotonic, hypertonic but N/S
Roy 1994
4
83 Yes Tone in shoulder rotators, elbow No Yes
exors, wrist exors and extensors:
on Ashworth Scale
Cheng 1995
44
50 Yes Increased tone and stretch reexes No Yes
Zorowitz 1995
95
20 No Yes
Wanklyn 1996
46
108 No Yes
Ikai 1998
65
75 No Yes
HSP, hemiplegic shoulder pain.
at PENNSYLVANIA STATE UNIV on June 5, 2014 cre.sagepub.com Downloaded from
282 L Turner-Stokes and D Jackson
per se.
41,44,48,56
However, it can be difcult to dis-
tinguish between active spasticity and capsular
adhesion/contracture both of which typically
result in a reduced range of external rotation in
the shoulder and a number of studies have
demonstrated a strong relationship between HSP
and reduced range of external rotation.
40,41,44,46,65
So how, exactly, might spasticity cause pain?
Braun et al.
2
postulate that spasticity in the shoul-
der girdle muscles, and particularly in subscapu-
laris which pulls the arm into medial rotation,
may cause pain by traction on the periosteum at
the muscle insertion. They reported relief of pain
in their series where muscular contracture was
surgically released but the capsular contracture
left intact.
2
To eliminate internal rotation and
adduction the subscapularis and pectoralis ten-
dons were transected in an initial series of 13
patients who presented with pain, limitation of
movement and spasticity.
66
Marked pain reduc-
tion and increase in range of movement were
observed in 10 patients. A follow-up study of 50
patients showed similar improvement in 88%.
2
A
study by Hecht
67
showed that similar results
could be obtained by phenolization of the nerves
to the subscapularis muscle, and together these
studies suggest that active spasticity at least plays
a part in the genesis of HSP.
Intracapsular inammation: adhesive capsulitis
or frozen shoulder
Hemiplegia has been associated with the devel-
opment of adhesive capsulitis
41,65,6870
and Table
3 summarizes the relationship between HSP and
soft tissue lesions, which include adhesive cap-
sulitis and rotator cuff tears.
Bruckner and Nye
68
report adhesive capsulitis
in 25% of their series of 91 patients, most of
whom had undergone neurosurgery for sub-
arachnoid haemorrhage, but they use this term
loosely to describe the clinical presentation of a
painful stiff shoulder from any cause. As seen
above, this picture could equally arise from spas-
ticity. On the other hand, prolonged immobiliza-
tion as a result of paralysis can also result in
secondary capsular contracture. In the series by
Ikai et al.,
65
23 patients had arthrograms of which
74% had a small capsular outline, which he inter-
preted as adhesive capsulitis, and there was a
marked correlation between severity of pain and
loss of external rotation. Rizk et al.
69
reported a
77% incidence of adhesive capsulitis in their
arthrographic series of 30, and likewise Hakuno
et al. noted a 55% incidence of adhesive changes,
although there was also a 33% incidence on the
unaffected side.
70
In the literature on hemiplegia, adhesive cap-
sulitis has been related to paralysis, unconscious-
ness, impingement and subluxation.
9
It is likely
also that it is a late sequel of chronic spasticity
but, given the failure in many studies to distin-
guish between active spasticity and capsular con-
tracture, it is once again hard to separate cause
and effect. On the basis of the above studies it
seems likely that spasticity plays a signicant role
in the pathogenesis of shoulder pain, even though
its effect may be obscured by subsequent con-
tracture and adhesions. Therapeutic intervention
targeted towards the reduction of spasticity in its
early stages, may therefore be an important fac-
tor in reducing HSP as well as maintaining joint
range in the anticipation of future functional
recovery.
Subluxation
In 1957, Tobis
59
put forward the suggestion
that the main cause of shoulder pain in hemiple-
gia is accidity, and that the weight of the unsup-
ported arm stretches the capsule and ligaments,
resulting in subluxation and pain. Since then,
there have been numerous attempts to link sub-
luxation with shoulder pain, some authors sup-
porting a relationship
4,33,56,63
and others disputing
it.
2,40,42,44,46,48,61,62,71
Those that present gures are
summarized in Table 4.
Once again, confusion arises from failure to
dene subluxation. Most commonly, the term
subluxation is used to imply inferior subluxa-
tion.
24,42,44,46,48,71,72
The term malalignment
4
or
pre-subluxation
73
is used by some to imply minor
degrees of incongruency and subluxation a
more major disturbance. Others use malalign-
ment to mean inferior subluxation.
33,74
Subluxa-
tion may also occur in different directions.
Flaccidity is commonly associated with down-
ward displacement, but in spasticity, the humeral
head may be displaced anteriorly, posteriorly or
in medial rotation. The direction of malalignment
is by no means always clear. Some use malalign-
ment as a general term to mean displacement in
at PENNSYLVANIA STATE UNIV on June 5, 2014 cre.sagepub.com Downloaded from
Shoulder pain after stroke 283
T
a
b
l
e

3
H
e
m
i
p
l
e
g
i
c

p
a
i
n

a
n
d

s
o
f
t
-
t
i
s
s
u
e

l
e
s
i
o
n
s
A
u
t
h
o
r
,
M
e
t
h
o
d

o
f
I
n
c
i
d
e
n
c
e

o
f
R
e
l
a
t
i
o
n
s
h
i
p

o
f
I
n
c
i
d
e
n
c
e

o
f
R
e
l
a
t
i
o
n
s
h
i
p

o
f
S
u
b
l
u
x
a
t
i
o
n
y
e
a
r
a
s
s
e
s
s
m
e
n
t
a
d
h
e
s
i
v
e
c
a
p
s
u
l
i
t
i
s

t
o

H
S
P
r
o
t
a
t
o
r

c
u
f
f
R
C

t
e
a
r
s

t
o

H
S
P
(
N
o
.

s
u
b
j
e
c
t
s
)
c
a
p
s
u
l
i
t
i
s
(
R
C
)

t
e
a
r
s
N
a
j
e
n
s
o
n
A
r
t
h
r
o
g
r
a
p
h
y
N
o
t

1
3

(
4
0
%
)
A
l
l

t
e
a
r
s

h
a
d

p
a
i
n
T
o
t
a
l

i
n
c
i
d
e
n
c
e
:

8
1
%
1
9
7
1
3
3
A
f
f
e
c
t
e
d

s
i
d
e

o
n
l
y
m
e
n
t
i
o
n
e
d
(
1
0
/
1
1

p
t
s

w
i
t
h
A
l
l

t
e
a
r
s

h
a
d

s
e
v
e
r
e
(
n
=

3
2
)
s
e
v
e
r
e

p
a
i
n

i
n

t
h
i
s
m
a
l
a
l
i
g
n
m
e
n
t
s
e
r
i
e
s

h
a
d

R
C

t
e
a
r
s
)
N
e
p
o
m
u
c
e
n
o
A
r
t
h
r
o
g
r
a
p
h
y
0

7

(
3
0
%
)
A
l
l

t
e
a
r
s

h
a
d

p
a
i
n
T
o
t
a
l

i
n
c
i
d
e
n
c
e
:

4
6
%
1
9
7
4
8
0
A
f
f
e
c
t
e
d

s
i
d
e

o
n
l
y
5
/
7

(
7
1
%
)

t
e
a
r
s

h
a
d
(
n
=

2
4
)
s
u
b
l
u
x
a
t
i
o
n
B
r
u
c
k
n
e
r
C
l
i
n
i
c
a
l
2
3

(
2
5
%
)
C
a
n
n
o
t

c
o
m
p
u
t
e
N
o
t

m
e
n
t
i
o
n
e
d

N
o

d
a
t
a

g
i
v
e
n
1
9
8
1
6
8
(
P
a
i
n
f
u
l

s
t
i
f
f
(
D
i
a
g
n
o
s
i
s

m
a
d
e

o
n
(
n
=

9
9
)
s
h
o
u
l
d
e
r
)
t
h
e

b
a
s
i
s

o
f

p
a
i
n
)
R
i
z
k
A
r
t
h
r
o
g
r
a
p
h
y
2
3

(
7
7
%
)
C
a
n
n
o
t

c
o
m
p
u
t
e
N
o
n
e

T
o
t
a
l

i
n
c
i
d
e
n
c
e
:

0
%
1
9
8
4
6
9
A
f
f
e
c
t
e
d

s
i
d
e

o
n
l
y
(
P
a
t
i
e
n
t
s

s
e
l
e
c
t
e
d

o
n
(
n
=

3
0
)
t
h
e

b
a
s
i
s

o
f

p
a
i
n
f
u
l
s
t
i
f
f

s
h
o
u
l
d
e
r
)
H
a
k
u
n
o
A
r
t
h
r
o
g
r
a
p
h
y
4
2

(
5
5
%
)
N
o
t

s
i
g
n
i

c
a
n
t
1
7

(
2
2
%
)
N
o
t

s
i
g
n
i

c
a
n
t
T
o
t
a
l

i
n
c
i
d
e
n
c
e

3
9
%
1
9
8
4
7
0
B
o
t
h

s
i
d
e
s
a
f
f
e
c
t
e
d

s
i
d
e
a
f
f
e
c
t
e
d

s
i
d
e
S
i
g
n
i

c
a
n
t
N
o

d
a
t
a

g
i
v
e
n

o
n
(
n
=

7
7
)
2
5

(
3
3
%
)
1
9

(
2
5
%
)
c
o
r
r
e
l
a
t
i
o
n

o
n
l
y

w
i
t
h
r
e
l
a
t
i
o
n
s
h
i
p

o
f

t
e
a
r
s

o
r
n
o
n
-
a
f
f
e
c
t
e
d
n
o
n
-
a
f
f
e
c
t
e
d
p
a
i
n

b
e
f
o
r
e

s
t
r
o
k
e
c
a
p
s
u
l
i
t
i
s

w
i
t
h
s
u
b
l
u
x
a
t
i
o
n
I
k
a
i
A
r
t
h
r
o
g
r
a
p
h
y
1
7

(
7
4
%
)
C
o
r
r
e
l
a
t
i
o
n

w
i
t
h
1

(
4
%
)

N
o

d
a
t
a

g
i
v
e
n
1
9
9
8
6
5
A
f
f
e
c
t
e
d

s
i
d
e

o
n
l
y
p
a
i
n

s
e
v
e
r
i
t
y

a
n
d
F
o
r

t
h
e

s
u
b
g
r
o
u
p

(
2
3
/
7
5
)
(
n
=

2
3
)
r
e
d
u
c
e
d

r
a
n
g
e

o
f
w
h
o

h
a
d

a
r
t
h
r
o
g
r
a
p
h
y
e
x
t
e
r
n
a
l

r
o
t
a
t
i
o
n
H
S
P
,

h
e
m
i
p
l
e
g
i
c

s
h
o
u
l
d
e
r

p
a
i
n
.
at PENNSYLVANIA STATE UNIV on June 5, 2014 cre.sagepub.com Downloaded from
284 L Turner-Stokes and D Jackson
other causes of shoulder pain in the various study
populations. In studies which formally assessed
the relationship of HSP with multiple variables,
there was a stronger relationship with spasticity
63
and with reduced range of external rotation than
with inferior subluxation.
40,41,44,65
Even though
any direction,
56
others use subluxation for this
purpose.
30,40,65
To confuse matters further, some
measured subluxation radiologically and some
just by clinical assessment (see Table 4).
One of the reasons for a variable relationship
with shoulder pain may be the failure to identify
Table 4 Reported incidence of subluxation and relationship to shoulder pain
Author and date No. in Subluxation Method of assessment of Position Relationship
series % subluxation to HSP
Najenson 1971
33
32 26 (81%) Radiological: AP radiograph Supine and erect Yes
Inferior subluxation only
Graded: I = subluxation,
II = luxation
Fitzgerald-Finch 100 17 (17%) Radiological: AP radiograph Erect in standing
1975
72
Inferior subluxation only: (Patients had to
Present or absent be able to stand)
Smith 1982
74
110 51 (46%) Radiological: AP radiograph Supine and erect
Inferior subluxation only
Graded: 03
Van Oewenaller 219 109 (50%) Radiological: AP radiograph Not specied Yes
1986
63
Inferior subluxation only:
Present or absent
Van Langenberghe 44 24 (54%) Radiological: AP radiograph Not specied No
1988
12
Inferior subluxation only
Graded: 04
Bohannon 1990
42
24 9 (37%) Clinical: Sitting (erect) No
Inferior subluxation only
Graded: 0, 1(minimal),
2(substantial)
Joynt 1992
48
67 21 (31%) Clinical Not specied No
Unspecied method
Ring 1993
56
80 45 (56%) Radiological: AP radiograph Sitting (erect) Yes
Inferior subluxation only:
Present or absent
Cheng 1995
44
50 23 (46%) Clinical:
Inferior subluxation only Not specied Yes
Present or absent
Roy 1994
4
76 26 (34%) Radiological: AP radiograph Unsupported arm Yes
Inferior subluxation only (presumed sitting)
Graded: 04
Zorowitz 1995
95
20 Correlation Radiological: AP radiograph Sitting No
reported rather Subluxation in two dimensions:
than incidence vertical and horizontal disparity
compared with normal side
Wanklyn 1996
46
108 13 (29%) Clinical: Sitting No
Inferior subluxation only
Graded in nger-breadths
Ikai 1998
65
75 Selected for Radiological: AP radiograph Sitting No
subluxation Subluxation in two dimensions:
as per Zorowitz 1995
at PENNSYLVANIA STATE UNIV on June 5, 2014 cre.sagepub.com Downloaded from
Shoulder pain after stroke 285
tunately, none of the reports describing the inci-
dence of subluxation and its relationship to HSP
used these techniques. Although Zorowitz et al.
40
refer to the methods described by Prevost,
32
they
actually use the simpler two-dimensional method
described by Brooke et al.
79
At the current time, clinical assessment by pal-
pation and erect X-rays taken in anterio-poste-
rior and oblique views as soon as this becomes
feasible are probably the mainstays for routine
assessment of subluxation.
Extracapsular inammation: rotator cuff tears
As has already been discussed under func-
tional anatomy, exion and abduction of the
shoulder must be accompanied by appropriate
rotation of the scapula and humeral head to
avoid impingement of the rotator cuff. The nor-
mal mechanisms that protect the rotator cuff are
lost in hemiplegia, and given that this group of
patients is also likely to have degenerative
changes predisposing to rotator cuff rupture, one
may suppose that trauma due to traction on lift-
ing and handling would be likely to damage the
rotator cuff and result in shoulder pain.
57
The
problem with relating cause and effect, however,
is the relatively high incidence of asymptomatic
tears in this population. Papers reporting a rela-
tionship between rotator cuff tears and shoulder
pain are summarized in Table 3.
Joynt
48
attempted to dene the source of HSP
by injecting 1% lignocaine into various sites in
the shoulder complex. Moderate or marked relief
was obtained by injection of the subacromial
bursa in about half of his 28 patients, suggesting
that subacromial pathology makes a signicant
contribution to HSP at least in a proportion of
cases.
Najenson et al.
33
concluded from arthrographic
studies on 32 patients that rotator cuff tears
were more common on the affected than the non-
affected side. They found rotator cuff tears in
40% of their patients, which were accompanied
in all cases by severe malalignment and pain.
Nepomuceno and Miller similarly found rotator
cuff tears in 30% of their group of 24 patients.
80
However, Hakuno et al. found no signicant dif-
ference between the affected and nonaffected
side in his series of 77,
70
Rizk et al. found no
rotator cuff lesions at all among their series of
one might expect the development of spasticity
to reduce subluxation, the evidence suggests that
it may become irreversible after a period, per-
sisting even after voluntary control or spasticity
have developed.
33
This may be due to over-
stretching of the capsule, ligaments and
supraspinatus and deltoid muscles
38
or rupture of
the rotator cuff
33,73
during the accid stage.
Therefore, while subluxation may not be associ-
ated with pain in the early stages of hemiplegia,
if it persists into the chronic spastic stage, or is
complicated by soft tissue damage, the associa-
tion with pain and limitation of movement may
be higher.
The rather confused picture of subluxation in
relation to HSP conrms the need for accurate
assessment. A number of clinical methods of
assessing subluxation have been proposed, and
include measuring arm-length discrepancy,
75
assessment of the subacromial space by palpation
or calipers
76
or the use of a thermoplastic jig.
77
Of these methods, palpation proves the most reli-
able,
75,76
but caliper measurement may be more
sensitive and also gives reliable results.
76
The
only method which gave unacceptable reliability
was the jig.
75,76
Shoulder subluxation may be missed radiolog-
ically unless the subject is X-rayed in the erect
position.
24,74
This is often difcult to achieve in
the earlier stages of stroke recovery. Shai et al.
73
report the appearance of a V-shaped space
between the humeral head and glenoid fossa on
a plain X-ray, as an early sign of subluxation.
This is conrmed by Arsenault et al.
78
to precede
the onset of pain, and may therefore offer
the opportunity for early diagnosis and interven-
tion before subluxation progress to soft tissue
damage.
Radiographic measurement offers the oppor-
tunity for more detailed assessment. Prevost et
al.
32
describes a three-dimensional X-ray tech-
nique which employs a mathematical formula to
two X-rays (one taken at 0 anterio-posterior,
and the other at 45 oblique). This showed a high
level of repeatability and correlated well with
clinical tests. More recently Boyd and Torrance
76
have advocated the use of a digitizer and com-
puter to quantify measurements from a single X-
ray, although this requires specialized equipment
to standardize the position of the patient. Unfor-
at PENNSYLVANIA STATE UNIV on June 5, 2014 cre.sagepub.com Downloaded from
286 L Turner-Stokes and D Jackson
pain in hemiplegia may result from entrapment
of the suprascapular nerve. This nerve arises
from the upper trunk of the brachial plexus and
courses down posteriorly, passing through the
suprascapular notch before dividing into sensory
branches, supplying the acromioclavicular and
glenohumeral joints, and motor branches supply-
ing the supraspinatus and infraspinatus muscles.
It is potentially vulnerable to entrapment at the
suprascapular notch, and it was suggested that
traction on the nerve might result from
malalignment of the scapula leading to HSP.
However, only three of their 30 patients had
increased latency on EMG on the affected side
and suprascapular nerve block did not com-
pletely relieve their pain, so it was concluded that
suprascapular entrapment was not a signicant
cause of shoulder pain. Nevertheless, the supras-
capular nerve provides some of the sensory sup-
ply to the shoulder and blockade may offer the
possibility of pain relief in some cases.
An alternative explanation for lower motor
neuron involvement offered by Bhala
82
many
years earlier may be pertinent namely the con-
cept of upper and lower motor neuron depen-
dence and the notion that lower motor neuron
degeneration may follow as a direct consequence
of a destructive lesion of the upper motor
neuron.
Autonomic dysfunction: reex sympathetic
dystrophy (RSD)
Reex sympathetic dystrophy (RSD) or shoul-
derhand syndrome
83
is also cited as a cause of
shoulder pain in stroke, occurring in 12.5% of a
population of 540 in a ve-year retrospective
study reported by Davis et al.
53
and in 28% of 219
patients in Van Ouwenallers study.
63
RSD usually appears within three months and
rarely later than ve months following stroke.
53
Clinical criteria for diagnosis include severe pain,
hyperaesthesia, vasomotor disturbance, oedema
and eventually atrophy in the skin and muscle of
the shoulder and hand. There is frequently pain
and limitation at the shoulder, wrist and
metacarpo-phalangeal joints, while the elbow is
spared.
53
The mechanism of autonomic dysfunction in
stroke is unknown. Some have postulated peri-
pheral triggers such as immobility and decreased
30,
69
and Ikai et al. found only one.
65
Tobis
59
considered that the traction forces in
GHJ subluxation contributed to rotator cuff
tears. It is possible that the capsular adhesions
and/or spasticity provide relative protection
against rotator cuff damage to which accid sub-
luxed shoulders are more prone, and the expla-
nation for these different results lies in the
different selected populations. Najenson et al.
33
recruited patients with severe paralysis and an
84% prevalence of subluxation, while Rizk et al.
69
specically selected patients with spasticity
resulting in a painful stiff shoulder. Three-quar-
ters of Ikais group had capsular restriction,
65
while Hakuno et al.,
70
appeared to have a more
equal mixture of subluxation and adhesive cap-
sulitis.
It should be noted that all these studies were
undertaken using arthrography, before the era of
MRI, and the question should now be re-
addressed in larger numbers, in the light of more
advanced and less invasive technology.
14
Neuropathic damage or entrapment
Damage to the upper trunk of the brachial
plexus has also been cited as a possible cause of
pain and subluxation in the hemiplegic shoul-
der.
36,37
Chino reported neuropathic responses in
the supraspinatus and deltoid muscles in 75% of
his hemiplegic population.
37
Once again, cause
and effect is unclear. It has been suggested that
a combination of accidity and trauma due to
careless handling are responsible for traction
injury to the brachial plexus
36
which may then
serve to enhance the subluxation.
Kingery and colleagues,
81
on the other hand,
cast doubt on the occurrence of brachial plexus
lesions in stroke as they failed to nd evidence
of the condition in their prospective study of 50
patients. They do not report, however, how many
of these had subluxation and their series is small.
It may serve only to indicate that the combina-
tion of subluxation and trauma sufcient to cause
this complication are fortunately relatively
uncommon.
Ring et al. suggested that downward subluxa-
tion may produce traction on the axillary nerve
as it winds round the surgical neck of the humeral
shaft.
56
Lee and Khunadorn
35
suggested that shoulder
at PENNSYLVANIA STATE UNIV on June 5, 2014 cre.sagepub.com Downloaded from
Shoulder pain after stroke 287
produce any data or references to substantiate
this statement. A recent pilot RCT
86
failed to
show benet from a shoulder positioning proto-
col but the numbers (n = 23) were too small to
be conclusive.
There is, however, some circumstantial evi-
dence. Wanklyn et al. reported that the preva-
lence of HSP increases during the rst few weeks
following discharge from hospital.
46
In that study,
development of shoulder pain was more common
in patients who needed help for transfers, and
nine carers admitted pulling on the hemiplegic
arm, despite having been warned not to do so.
Ring et al.
56
reported that some referring hospi-
tals had consistently high rates of HSP while oth-
ers had a much lower rate. These differences
could not be accounted for by other factors such
as age, long waiting periods, etc., and so were
attributed to poor handling techniques.
So while there is no irrefutable evidence that
poor handling and incorrect positioning results in
increased likelihood of HSP, the weight of pro-
fessional opinion is such that a controlled trial of
best practice against worst practice would be
unethical. The question, therefore, is not whether
best practice should be applied, but what exactly
is considered to be best practice?
Carr and Kenney
87
explored recommendations
in the literature for positioning in both lying and
sitting. There was general concurrence that the
shoulder should be protracted (to avoid retrac-
tion), the arm forward, the wrist in neutral or
slight supination, and the ngers extended. Opin-
ion was divided on whether the elbow should be
exed or extended, and whether the arm should
be abducted and externally rotated or not. Their
article provides an admirably systematic review
of prevailing opinion, but fails to recognize the
need for all of us to change position from time
to time, and thus the need for a range of
approved changes within each overall position
as is recommended by others.
13
Static positioning is all very well when the
patient is, so to speak, a captive audience, but as
they improve and get up on their feet, the pull of
gravity puts a further vertical load on the accid
shoulder and the need for more mobile support
must be considered.
sensory input causing an imbalance in central
neural control of the sympathetic system.
84
Oth-
ers have suggested that the central lesion itself
may be responsible.
85
A plain radiograph may
show patchy demineralization, but the most spe-
cic diagnostic test is a technetium diphos-
phonate bone scan, which shows increased
peri-articular uptake, particularly at the shoulder
and wrist.
1
Tepperman et al.
43
found evidence of RSD on
bone scan in 21/85 (25%) of hemiplegic patients,
although only two-thirds went on to develop the
clinical syndrome. This suggests that many fea-
tures associated with RSD, such as oedema, wast-
ing and exural contracture may be secondary
features associated with immobility and might
explain the confusion in the literature between
RSD and shoulderhand syndrome. In this con-
text, therefore, criteria for the diagnosis of RSD
should include vasomotor changes such as
changes in skin colour, temperature and sweat-
ing, and MCP tenderness. Under this stricter def-
inition, it is probably less common than the
literature suggests. Nevertheless, its importance
lies in the fact that specic intervention targeted
at the sympathetic nervous system may become
appropriate if the diagnosis is conrmed.
The evidence for effectiveness of
different interventions in the
management of HSP
Because of the diverse and multifactorial aetiol-
ogy of HSP, management is often difcult and the
result of treatment unsatisfactory. In this last sec-
tion we review the evidence for effectiveness of
different interventions in the management of
HSP.
Positioning and handling
Many authors have suggested that trauma to
the shoulder joint can be prevented by proper
positioning and handling.
3,24,29,33,56,57,61,62,72
How-
ever, much of this comment is speculative only
rotator cuff tears have been subjected to formal
review as evidence for this statement.
12
Moskowitz et al.
24
report that with proper posi-
tioning and handling the incidence of HSP can be
reduced from 75% to as low as 5%, but do not
at PENNSYLVANIA STATE UNIV on June 5, 2014 cre.sagepub.com Downloaded from
288 L Turner-Stokes and D Jackson
tant subluxation. In general, arm slings appear to
provide the best correction of subluxation, both
in vertical
79,93
and horizontal
79
planes. They may
also prevent the accid arm from banging against
the body during functional activities
27
and be use-
ful as a temporary support during early gait re-
education.
93,94
However, many authors express
reservations about the long-term use of slings
which immobilize the arm in exion, adduction
and internal rotation.
Axillary supports such as the Bobath sling or
roll,
79,90,93,95,96
consist of a covered foam roll posi-
tioned in the axilla and anchored with straps over
the shoulders or around the body. The design is
discreet and does not encourage exor posturing
or limit movement of the arm. Originally
intended for use by patients with adductor spas-
ticity,
93
the axillary roll has since been evaluated
as a support for the subluxed humerus, but unfor-
tunately with poor results. Not only does it fail
to correct subluxation to an acceptable
degree,
79,90,93,95,96
it also produces lateral displace-
ment of the humeral head
79,95
thus increasing
stress on soft tissues.
90
Increasing recognition of
this problem has probably been one of the main
reasons for the decline in popularity of the axil-
lary roll over recent years.
94
Humeral cuff supports attempt to emulate the
deltoid muscle by pulling the humeral head up
from above. They consist of an adjustable cuff
around the upper part of the affected arm held
in place by a gure of eight body harness as in
the Roylan type
27,95
or a bilateral cuff joined by
a yoke across the back as in the Hook hemi-har-
ness.
93
Zorowitz et al. found the Roylan sling
allowed slight external rotation of the shoulder
when optimally applied and it provided the best
total reduction in subluxation.
95
This type of sup-
port was felt to be most appropriate for patients
with some volitional movement. In contrast, the
Hook hemi-harness was ineffective, restrictive to
movement and uncomfortable to wear.
93
Evidence suggests, therefore, that different
supports suit individuals at different stages in
recovery making careful evaluation essential to
optimize function of the affected limb and reduce
subluxation.
95
However, no study to date has for-
mally addressed the reliability of everyday appli-
cation by ward staff or carers. Simplicity in
application may be as important as the intrinsic
Slings and supports
Slings and supports are frequently used in the
management of a hemiplegic patient to reduce
subluxation and protect the arm from trauma.
However, their use remains controversial. Not
only are they sometimes ineffective,
88
they can
also reduce upper limb mobility and sensory
input, encourage exor tone, and impair gait and
body image.
7
Slings are often applied incorrectly
or discarded by patients.
89
For these reasons, it is
important not only to consider what congura-
tion provides the best arm position, but also who
is going to put it on and whether it will actually
be worn.
6
A number of studies have explored the bio-
mechanical effects of different slings
9092
with a
view to helping therapists to identify the
patients particular condition and the sling which
might be most appropriate. Others have made
direct radiographic comparisons of the effects of
different types of sling in the same patients, but
only one group
93
suggest an acceptable level for
correction of inferior subluxation as within 0.5
cm of the normal (unaffected) side. The details
of these studies are listed in Table 5.
For chair-bound patients, an arm trough or lap
tray can provide support for a accid arm and
effective reduction of subluxation,
79,93
while posi-
tioning the arm away from the body, discourag-
ing adduction and internal rotation
79
and
allowing bilateral upper limb activities.
93
Their
downside is a tendency to over-correct subluxa-
tion,
79,93
especially if the patient slips down in the
chair,
91
though careful choice of seating and reg-
ular monitoring of patients should overcome this
problem.
94
Both demonstrate a lesser tendency to
wander than the ordinary pillow. An arm trough
is more likely to permit independent transfers
than a lap tray, but naturally, both become inef-
fective as soon as the patient starts to spend sig-
nicant periods of time on their feet and out of
their chair.
Worn support devices broadly divide into three
types: arm slings, axillary supports and humeral
cuff supports. Arm slings may have contralat-
eral
95
or bilateral
79
supporting shoulder straps but
the rationale for both types is the same, being to
support the forearm and distribute its weight to
one or both shoulders, thus preventing or reduc-
ing stretch to the shoulder capsule and any resul-
at PENNSYLVANIA STATE UNIV on June 5, 2014 cre.sagepub.com Downloaded from
Shoulder pain after stroke 289
T
a
b
l
e

5
S
l
i
n
g
s

a
n
d

s
u
p
p
o
r
t
s

i
n

t
h
e

m
a
n
a
g
e
m
e
n
t

o
f

s
u
b
l
u
x
a
t
i
o
n
A
u
t
h
o
r
,

y
e
a
r
A
s
s
e
s
s
m
e
n
t
D
e
v
i
c
e
s

u
s
e
d
C
o
r
r
e
c
t
i
o
n

o
f

s
u
b
l
u
x
a
t
i
o
n
O
v
e
r
a
l
l

c
o
n
c
l
u
s
i
o
n
N
o
.

o
f

s
u
b
j
e
c
t
s
m
e
t
h
o
d
s
M
e
a
n

d
i
f
f
e
r
e
n
c
e

f
r
o
m
u
n
a
f
f
e
c
t
e
d

a
r
m

(
c
m
)
M
o
o
d
i
e

1
9
8
6
9
3
A
P

r
a
d
i
o
g
r
a
p
h
T
r
i
a
n
g
u
l
a
r

b
a
n
d
a
g
e

0
.
0
2

(
v
e
r
t
i
c
a
l
)
E
f
f
e
c
t
i
v
e

(
b
u
t

i
m
m
o
b
i
l
i
z
e
d

t
h
e

a
r
m
)
(
n
=

1
0
)
I
n
f
e
r
i
o
r

s
u
b
l
u
x
a
t
i
o
n
o
n
l
y
B
o
b
a
t
h

r
o
l
l
0
.
6
4

(
v
e
r
t
i
c
a
l
)
I
n
e
f
f
e
c
t
i
v
e

(
u
n
d
e
r
c
o
r
r
e
c
t
e
d
)
H
o
o
k

h
e
m
i
-
h
a
r
n
e
s
s
0
.
9
8

(
v
e
r
t
i
c
a
l
)
I
n
e
f
f
e
c
t
i
v
e

(
u
n
d
e
r
c
o
r
r
e
c
t
e
d
)
L
a
p
-
t
r
a
y

0
.
1
6

(
v
e
r
t
i
c
a
l
)
E
f
f
e
c
t
i
v
e

(
b
u
t

o
v
e
r
c
o
r
r
e
c
t
e
d

i
n

s
o
m
e

c
a
s
e
s
)
A
r
m

t
r
o
u
g
h
0
.
0
7

(
v
e
r
t
i
c
a
l
)
E
f
f
e
c
t
i
v
e

(
b
u
t

o
v
e
r
c
o
r
r
e
c
t
e
d

i
n

s
o
m
e

c
a
s
e
s
)
W
i
l
l
i
a
m
s

1
9
8
8
9
6
A
P

r
a
d
i
o
g
r
a
p
h
B
o
b
a
t
h

r
o
l
l
0
.
8
2

(
v
e
r
t
i
c
a
l
)
B
e
t
t
e
r

t
h
a
n

n
o

s
u
p
p
o
r
t
.

C
o
m
f
o
r
t
a
b
l
e

t
o

w
e
a
r
(
n
=

2
6
)
I
n
f
e
r
i
o
r

s
u
b
l
u
x
a
t
i
o
n
o
n
l
y
H
e
n
d
e
r
s
o
n

s
l
i
n
g
0
.
8
8

(
v
e
r
t
i
c
a
l
)
B
e
t
t
e
r

t
h
a
n

n
o

s
u
p
p
o
r
t
.

C
o
m
f
o
r
t
a
b
l
e

t
o

w
e
a
r
Z
o
r
o
w
i
t
z

1
9
9
5
9
5
A
P

r
a
d
i
o
g
r
a
p
h
S
i
n
g
l
e

s
t
r
a
p

h
e
m
i
-
s
l
i
n
g
0
.
3
4

(
v
e
r
t
i
c
a
l
)
E
f
f
e
c
t
i
v
e

i
n

v
e
r
t
i
c
a
l

a
n
d

h
o
r
i
z
o
n
t
a
l

p
l
a
n
e
s
.
(
n
=

2
0
)
V
e
r
t
i
c
a
l

a
n
d
0
.
0
0

(
h
o
r
i
z
o
n
t
a
l
)
B
e
s
t

v
e
r
t
i
c
a
l

c
o
r
r
e
c
t
i
o
n

i
n

5
5
%

o
f

p
a
t
i
e
n
t
s
h
o
r
i
z
o
n
t
a
l
B
o
b
a
t
h

r
o
l
l
0
.
6
2

(
v
e
r
t
i
c
a
l
I
n
e
f
f
e
c
t
i
v
e

(
l
a
t
e
r
a
l

d
i
s
p
l
a
c
e
m
e
n
t

o
f

h
u
m
e
r
a
l

h
e
a
d
)
d
i
s
p
l
a
c
e
m
e
n
t
.
0
.
4
9

(
h
o
r
i
z
o
n
t
a
l
)
B
e
s
t

v
e
r
t
i
c
a
l

c
o
r
r
e
c
t
i
o
n

i
n

2
0
%

o
f

p
a
t
i
e
n
t
s
A
l
s
o

c
a
l
c
u
l
a
t
e
d
R
o
y
l
a
n

h
u
m
e
r
a
l

c
u
f
f

s
l
i
n
g
0
.
5
8

(
v
e
r
t
i
c
a
l
)
E
f
f
e
c
t
i
v
e

(
b
e
s
t

r
e
d
u
c
t
i
o
n

i
n

t
o
t
a
l

a
s
s
y
m
e
t
r
y
)
t
o
t
a
l

s
u
b
l
u
x
a
t
i
o
n
0
.
1
5

(
h
o
r
i
z
o
n
t
a
l
)
B
e
s
t

v
e
r
t
i
c
a
l

c
o
r
r
e
c
t
i
o
n

i
n

4
0
%

o
f

p
a
t
i
e
n
t
s
.

a
s
y
m
m
e
t
r
y
C
a
v
a
l
i
e
r
0
.
9
0

(
v
e
r
t
i
c
a
l
)
I
n
e
f
f
e
c
t
i
v
e

(
u
n
d
e
r
c
o
r
r
e
c
t
e
d

i
n

v
e
r
t
i
c
a
l

p
l
a
n
e

a
n
d
0
.
4
6

(
h
o
r
i
z
o
n
t
a
l
)
c
a
u
s
e
d

l
a
t
e
r
a
l

d
i
s
p
l
a
c
e
m
e
n
t

o
f

h
u
m
e
r
a
l

h
e
a
d
)
B
r
o
o
k
e

1
9
9
1
7
9
A
P

r
a
d
i
o
g
r
a
p
h
H
a
r
r
i
s

s
l
i
n
g

0
.
0
7

(
v
e
r
t
i
c
a
l
)
B
e
s
t

v
e
r
t
i
c
a
l

c
o
r
r
e
c
t
i
o
n

a
n
d

m
o
s
t

c
o
n
s
i
s
t
e
n
t
(
n
=

1
0
)
V
e
r
t
i
c
a
l

a
n
d

0
.
1
6

(
h
o
r
i
z
o
n
t
a
l
)
h
o
r
i
z
o
n
t
a
l
B
o
b
a
t
h

s
l
i
n
g
0
.
4
7

(
v
e
r
t
i
c
a
l
)
L
e
s
s

e
f
f
e
c
t
i
v
e

v
e
r
t
i
c
a
l

c
o
r
r
e
c
t
i
o
n

a
n
d

d
i
s
t
r
a
c
t
e
d

t
h
e
d
i
s
p
l
a
c
e
m
e
n
t
0
.
6
6

(
h
o
r
i
z
o
n
t
a
l
)
g
l
e
n
o
h
u
m
e
r
a
l

j
o
i
n
t

i
n

t
h
e

h
o
r
i
z
o
n
t
a
l

p
l
a
n
e
A
r
m

t
r
o
u
g
h
/
l
a
p
-
t
r
a
y

0
.
7
8

(
v
e
r
t
i
c
a
l
)
L
e
s
s

e
f
f
e
c
t
i
v
e
;

t
e
n
d
e
d

t
o

o
v
e
r
c
o
r
r
e
c
t
.

A
r
m

c
o
u
l
d

b
e
0
.
0
6

(
h
o
r
i
z
o
n
t
a
l
)
p
o
s
i
t
i
o
n
e
d

i
n

l
e
s
s

a
d
d
u
c
t
i
o
n

a
n
d

l
a
t
e
r
a
l

r
o
t
a
t
i
o
n
at PENNSYLVANIA STATE UNIV on June 5, 2014 cre.sagepub.com Downloaded from
290 L Turner-Stokes and D Jackson
rotation
100
) is suggested as a realistic goal.
Reduction of muscle tone prior to passive ele-
vation of the spastic shoulder is recommended.
61
For example, where spasticity pulls the arm into
internal rotation, this must be reversed before the
arm is abducted beyond 90. Equally, in the sub-
luxed shoulder, the humeral head should be relo-
cated in the glenoid cavity before movement to
avoid traction damage.
59
A variety of physio-
therapy techniques have been described
61,62
many
of which are aimed at restoring normal alignment
and inhibiting muscle tone in the muscle groups
which produce shoulder retraction but their
detailed description is beyond the scope of this
review. Some success has also been reported with
antispasmodic drugs
63
and with ice and heat.
62,63,69
Electrical stimulation
The role of functional electrical stimulation
(FES) in management of both the upper and
lower limb following stroke was reviewed by
Binder-Macleod and Lee
101
and its role in the
management of HSP is currently the subject of a
Cochrane systematic review.
102
In the meantime, we summarize ve controlled
trials of FES in the management of the hemi-
plegic shoulder (Table 6). FES aims to maintain
muscle bulk and tone in the accid shoulder and
possibly enhance functional recovery through
cortical feedback. Some have used FES to pre-
vent the development of subluxation in the ac-
cid shoulder,
103,104
while others aim for reversal of
existing subluxation.
105107
FES has been applied
either to the posterior deltoid and supraspinatus
muscles,
107
or to both,
103,104,106
except in
Chantraines study
105
which did not specify a site.
Stimulation was continued for between four and
six weeks but the actual regimen and number of
hours per day varied markedly between studies.
Overall, FES produced encouraging effects on
subluxation, both for treatment and prophylaxis.
Some also reported improvement in motor func-
tion,
104,105,107
although where specied, this was
mainly power of abduction. The relationship with
actual pain was not so clear, but three of the ve
studies reported some degree of improvement in
HSP.
104,105,107
Linn et al.
103
expressed concern that
the effects did not last after FES was discontin-
ued. However, their study used the shortest reg-
imen (four weeks). Chantraines larger study
105
properties of the sling. Moreover, slings and sup-
ports may reduce subluxation, but do they actu-
ally reduce hemiplegic shoulder pain? The only
study to address this directly was a small prospec-
tive study of strapping,
97
which showed that the
onset of HSP could be delayed in a population
of patients with new strokes.
To overcome the problem of compliance,
Pinzur and Hopkins
98
have promoted an opera-
tion to reduce inferior subluxation by looping the
long tendon of biceps over the coracoid process.
This was reported to provide complete pain relief
in 5/6 patients. However, this is clearly something
to be considered only in chronic accidity, and
not while there is any possibility that spasticity
will still develop.
In summary, given the evidence that severe
subluxation may result in damage to soft tissues
and possibly even nerves, and given the intuitive
notion that a supported arm is less likely to be
exposed to forces which produce subluxation,
best practice would appear to advocate that the
arm should be supported around the clock by
whichever method provides the best correction in
that individual. If nothing else, a sling or support
may serve to alert staff to the need to handle the
arm with care.
Passive range of movement and reduction of
spasticity
Early passive range exercise is generally
agreed to be an important measure to prevent
immobility and soft tissue contracture.
10
Again,
the question is not whether it should be done, but
how? Improperly administered passive exercise,
however, can cause impingement. The use of
overhead exercise pulleys, in particular, has been
cited as a cause of pain, impingement and even
rotator cuff rupture
33
and has been positively
associated with the development of HSP
99
they
should not, therefore, be used. Instead, passive
range exercises should be undertaken by a
trained professional to ensure that the shoulder
is moved with appropriate rotation of the scapula
and humerus to avoid impingement or damage to
the rotator cuff. It is important to remember,
however, that normal range becomes reduced in
an older population.
20
Maintenance of a free
functional range of movement (100 exion, 90
abduction, 30 lateral rotation, and 70 medial
at PENNSYLVANIA STATE UNIV on June 5, 2014 cre.sagepub.com Downloaded from
Shoulder pain after stroke 291
T
a
b
l
e

6
T
h
e

u
s
e

o
f

F
E
S

i
n

t
h
e

m
a
n
a
g
e
m
e
n
t

o
f

H
S
P

a
n
d

s
u
b
l
u
x
a
t
i
o
n
A
u
t
h
o
r

a
n
d
N
o
.

o
f

s
u
b
j
e
c
t
s
T
i
m
e

a
f
t
e
r
D
e
s
i
g
n
I
n
t
e
n
t
i
o
n
R
e
g
i
m
e
n
M
u
s
c
l
e
s
S
i
g
n
i

c
a
n
t

e
f
f
e
c
t
s
y
e
a
r
S
e
l
e
c
t
i
o
n
s
t
r
o
k
e

o
n
s
e
t
f
o
l
l
o
w
-
u
p
B
a
k
e
r
1
9
8
6
1
0
6
n
=

6
3
2

3
6

w
e
e
k
s
R
C
T
T
r
e
a
t
m
e
n
t

o
f
I
n
c
r
e
a
s
i
n
g

t
o
P
o
s
t
.

d
e
l
t
o
i
d
S
u
b
l
u
x
a
t
i
o
n
S
u
b
l
u
x
a
t
i
o
n
A
v
e
r
a
g
e

5

7
3
1

t
r
e
a
t
m
e
n
t
s
u
b
l
u
x
a
t
i
o
n
6

h
o
u
r
s
/
d
a
y

f
o
r
A
N
D
(
R
a
d
i
o
g
r
a
p
h
i
c
)
3
2

c
o
n
t
r
o
l
s
6

w
e
e
k
s
s
u
p
r
a
s
p
i
n
a
t
u
s
F
U
:

3

m
o
n
t
h
s
F
a
g
h
r
i
n
=

2
6
M
e
a
n

1
7

d
a
y
s
R
C
T
P
r
o
p
h
y
l
a
x
i
s
I
n
c
r
e
a
s
i
n
g

t
o
P
o
s
t
.

d
e
l
t
o
i
d
S
u
b
l
u
x
a
t
i
o
n
1
9
9
4
1
0
4
F
l
a
c
c
i
d
1
3

t
r
e
a
t
m
e
n
t
6

h
o
u
r
s
/
d
a
y

f
o
r
A
N
D
(
R
a
d
i
o
g
r
a
p
h
i
c
)
s
h
o
u
l
d
e
r
1
3

c
o
n
t
r
o
l
s
6

w
e
e
k
s
s
u
p
r
a
s
p
i
n
a
t
u
s
P
a
i
n
w
e
a
k
n
e
s
s
F
U
:

3

m
o
n
t
h
s
(
P
a
i
n
l
e
s
s

R
O
M

i
n
e
x
t
e
r
n
a
l

r
o
t
a
t
i
o
n
)
M
o
t
o
r
(
B
o
b
a
t
h

s
c
a
l
e
s
)
L
i
n
n
n
=

4
0
W
i
t
h
i
n

2

d
a
y
s
R
C
T
P
r
o
p
h
y
l
a
x
i
s
I
n
c
r
e
a
s
i
n
g
P
o
s
t
.

d
e
l
t
o
i
d
S
u
b
l
u
x
a
t
i
o
n
1
9
9
9
1
0
3
F
l
a
c
c
i
d
2
0

t
r
e
a
t
m
e
n
t
2

4

h
o
u
r
s
/
d
a
y
A
N
D
(
R
a
d
i
o
g
r
a
p
h
i
c
)
s
h
o
u
l
d
e
r
2
0

c
o
n
t
r
o
l
s
f
o
r

4

w
e
e
k
s
s
u
p
r
a
s
p
i
n
a
t
u
s
(
S
i
g
n
i

c
a
n
t

a
t

6

w
e
e
k
s
,
w
e
a
k
n
e
s
s
F
U
:

3

m
o
n
t
h
s
b
u
t

n
o
t

a
t

1
2

w
e
e
k
s
)
C
h
a
n
t
r
a
i
n
e
n
=

1
2
0
1
4

2
8

d
a
y
s
R
C
T
T
r
e
a
t
m
e
n
t

o
f
I
n
c
r
e
a
s
i
n
g
?
S
u
b
l
u
x
a
t
i
o
n
1
9
9
9
1
0
5
S
u
b
l
u
x
a
t
i
o
n
6
0

t
r
e
a
t
m
e
n
t
s
u
b
l
u
x
a
t
i
o
n
2

3

h
o
u
r
s
/
d
a
y
(
R
a
d
i
o
g
r
a
p
h
i
c
)
w
i
t
h

p
a
i
n
6
0

c
o
n
t
r
o
l
s
f
o
r

5

w
e
e
k
s
P
a
i
n
F
U
:

2

y
e
a
r
s
(
V
A
S

a
n
d

r
e
p
o
r
t
e
d
)
M
o
t
o
r

(
A
c
t
i
v
e

a
n
t
e
p
u
l
s
i
o
n

6
0

a
n
d

a
b
d
u
c
t
i
o
n

4
0

)
K
o
b
a
y
a
s
h
i
n
=

1
7
6
0

1
9
0

w
e
e
k
s
R
C
T
T
r
e
a
t
m
e
n
t

o
f
3
0

m
i
n
/
d
a
y
P
o
s
t
.

d
e
l
t
o
i
d
S
u
b
l
u
x
a
t
i
o
n
1
9
9
9
1
0
7
S
u
b
l
u
x
a
t
i
o
n
6

d
e
l
t
o
i
d
s
u
b
l
u
x
a
t
i
o
n
f
o
r

6

w
e
e
k
s
O
R
(
R
a
d
i
o
g
r
a
p
h
i
c
)
B
u
t

s
o
m
e
6

s
u
p
r
a
s
p
i
n
a
t
u
s
s
u
p
r
a
s
p
i
n
a
t
u
s
P
a
i
n
m
o
v
e
m
e
n
t
5

c
o
n
t
r
o
l
s
(
V
A
S

o
n

a
b
d
u
c
t
i
o
n
)
F
U
:

3

m
o
n
t
h
s
M
o
t
o
r
(
M
a
x
i
m
u
m

f
o
r
c
e

o
f
a
b
d
u
c
t
i
o
n
)
F
U
,

f
o
l
l
o
w
-
u
p
;

R
C
T
,

r
a
n
d
o
m
i
z
e
d

c
o
n
t
r
o
l

t
r
i
a
l
;

F
E
S
,

f
u
n
c
t
i
o
n
a
l

e
l
e
c
t
r
i
c
a
l

s
t
i
m
u
l
a
t
i
o
n
;

H
S
P
,

h
e
m
i
p
l
e
g
i
c

s
h
o
u
l
d
e
r

p
a
i
n
;

R
O
M
,

r
a
n
g
e

o
f

m
o
v
e
m
e
n
t
;
V
A
S
,

v
i
s
u
a
l

a
n
a
l
o
g
u
e

s
c
a
l
e
.
at PENNSYLVANIA STATE UNIV on June 5, 2014 cre.sagepub.com Downloaded from
292 L Turner-Stokes and D Jackson
peutic trial of NSAIDs, providing there are no
contraindications. Analgesic medication should
be withdrawn if not effective.
Local injection techniques
A recent survey from the Netherlands demon-
strated that most doctors believe that steroid
injections are effective in HSP.
110
In reality, local
injection with corticosteroids is shown to give dis-
appointing results in HSP, unless used specically
in the context of inammatory lesions such as
rotator cuff or bicipital tendinitis, or tears with
secondary subacromial bursitis. Modest relief has
been obtained by injection of the subacromial
bursa in some cases
48
presumably where rota-
tor cuff impingement or inammation was one of
the factors contributing to pain.
Dekker et al.
113
obtained some reduction of
pain with intra-articular injection of triamci-
nolone acetonamide in ve of their seven patients
in an AB design study, but elsewhere the disap-
pointing results from intra-articular steroid injec-
tion have been attributed to pain resulting from
spasticity in the shoulder girdle muscles
2
as
opposed to inammatory causes within the joint
cavity.
The popularity of local steroid injection prob-
ably reects a misheld assumption that HSP
arises from the same inammatory pathology that
gives rise to shoulder pain in the normal popula-
tion, i.e. adhesive capsulitis and rotator cuff ten-
dinitis. In the course of this review, however, we
have presented evidence for a range of other aeti-
ological factors for HSP (malalignment, spastic-
ity, etc.) which would not respond to the local
anti-inammatory effects of corticosteroid injec-
tion. In view of the likelihood that the atrophic
effects of repeated steroid injections will further
weaken the cuff, we conclude that this form of
treatment should only be employed with extreme
judiciousness. Symptomatic relief with an initial
test injection of lignocaine, or the use of T2-
weighted MRI images
14
may help to target
inammatory lesions and ensure that steroids are
only used where they are most likely to help.
The suprascapular nerve provides some of the
sensory innervation of the shoulder. Suprascapu-
lar nerve block has been used with some success
in relieving resistant shoulder pain in rheumatoid
arthritis,
114
persistent rotator cuff lesions
115
and in
had the longest follow-up period (two years) and
here the treatment effects were still evident for
pain, subluxation and shoulder mobility.
In a small study by Leandri et al.
108
high inten-
sity transcutaneous electrical stimulation (TENS)
was more effective in increasing range of move-
ment than either low-intensity TENS or placebo
stimulation, but the effect on pain was not com-
mented upon. Prada and Tallis
109
have used a
contingency electrical stimulator in the manage-
ment of neglect. Whenever the patient moves the
nonaffected arm, the device stimulates the fore-
arm skin to draw attention to the affected arm.
Preliminary results are promising, so if neglect
does have any part to play in the causation of
HSP, this might have a useful future role to play.
In summary, while the results of the formal sys-
tematic review are still awaited, FES appears to
offer potential benets, as an addendum to nor-
mal therapy, for both the treatment, and proba-
bly the prevention, of subluxation and its
complications. The jury is still out, however, on
other applications of electrical stimulation.
Oral analgesic medication
Giving symptomatic pain relief through the use
of simple analgesics or nonsteroidal anti-inam-
matory drugs (NSAIDs) is common practice in
the management of shoulder disorders both in
the general population
22
and in patients with
HSP.
11,110
Efcacy of NSAIDs for short-term
management of shoulder pain in general has been
suggested by the results of a systematic review of
19 trials.
111
The authors found a superior benet
over placebos in four trials, though differing
selection criteria and a wide range of shoulder
disorders meant that evidence of benet in spe-
cic pathologies could not be shown. However,
Green et al.
112
were unable to support these nd-
ings in a later systematic review of 31 trials inves-
tigating a range of interventions including
NSAIDs. They made more direct comparisons
between trials by calculating effect sizes for the
same reported outcome measures and concluded
that there is little evidence to either support or
refute the efcacy of common interventions for
shoulder pain.
In the absence of clear evidence for the ef-
cacy of NSAIDs and simple analgesia in HSP, it
seems reasonable to offer the individual a thera-
at PENNSYLVANIA STATE UNIV on June 5, 2014 cre.sagepub.com Downloaded from
Shoulder pain after stroke 293
Conclusions and proposed best
practice for management of HSP
Despite the substantial attention paid to hemi-
plegic shoulder pain in the literature it is still
poorly understood and often inadequately
treated. The purpose of this review was to clar-
ify the mechanisms that produce hemiplegic
shoulder pain and to examine the available evi-
dence that informs best practice in the manage-
ment of this difcult problem. So what
conclusions have we drawn?
Patients at high risk for developing HSP
appear to be those with severe paralysis in the
upper limb. Inappropriate handling techniques
may increase the likelihood of traction injury,
especially in the accid shoulder, and where
degenerative change in the rotator cuff predis-
poses to trauma. Education of all staff and rela-
tives involved in handling the patient is vital to
prevent damage that may prolong hospital stay
and increase disability. Careful hand-over to
community-based carers following discharge
from hospital is also essential. Because of the
diverse and multifactorial nature of HSP, suc-
cessful treatment depends on careful evaluation
and interpretation of the clinical signs with due
regard to the functional anatomy. While HSP
frozen shoulder.
116
In the only study currently in
the literature to use this technique in HSP
35
it
failed to provide complete pain relief. However,
it was used as a diagnostic test, rather than a
therapeutic manoeuvre, and in only three cases.
Suprascapular nerve block is a simple, safe and
inexpensive technique. In view of its potential,
demonstrated in other contexts, to relieve pain
originating from the shoulder, a therapeutic role
in HSP is worthy of further exploration.
As described above, reex sympathetic dystro-
phy (RSD) represents a specic subgroup of
HSP, requiring specic management in its own
right. Sympathetic blockade by stellate ganglion
block followed by intensive rehabilitation is cited
as the most effective treatment by earlier
authors
84,117
with surgical sympathectomy in
refractory cases.
84
More recently, Braus et al.
118
reported relief in 31/36 cases with low-dose oral
corticosteroids and this nding was supported by
a recent systematic review.
119
Hamamci et al.
120
reported a signicant reduction in pain and
increased range of movement in 25 patients
treated with salmon calcitonin, compared with 16
control subjects. Once again formal controlled
studies are needed, but preliminary reports of
success using noninvasive techniques merit fur-
ther investigation.
The clear relationship between spasticity and
shoulder pain, and the response of spastic shoul-
der pain to surgical release
2
(in resistant cases)
and similarly to subscapular nerve block
67
sug-
gests that this is an area worthy of further explo-
ration. Botulinum toxin has been used on other
sites of the body to reduce localized spasticity
with good effect.
121
To date there has been no
formal trial of botulinum toxin injected into the
subscapularis, possibly because of the expense of
the agent and the relative technical difculty of
siting an injection. However, there is clearly a
need for further study in this area.
In summary, local steroid injections either to
the glenohumeral joint or the subacromial bursa
should be avoided unless there is clear evidence
of an inammatory lesion. Nerve blocks may
have a role to play in reduction of severe pain or
sympatho-mimetic symptoms, and in spasticity
management the role for botulinum toxin needs
further exploration. These and other less invasive
techniques require systematic evaluation.
Clinical messages
Hemiplegic shoulder pain (HSP) is an
important condition, requiring co-ordinated
multidisciplinary management to minimize
interference with rehabilitation and opti-
mize outcome.
HSP broadly divides into accid and spas-
tic presentations each requiring different
approaches to handling, support and inter-
vention. Management should vary accord-
ingly.
Education of all staff and relatives involved
in handling the patient is vital to prevent
damage that may prolong hospital stay and
increase disability.
Development of an ICP provides a method-
ical approach to management and a sound
basis for prospective evaluation of interven-
tions in the future.
at PENNSYLVANIA STATE UNIV on June 5, 2014 cre.sagepub.com Downloaded from
294 L Turner-Stokes and D Jackson
traindications. Caution must be exercised for
those with a history of peptic ulceration, those
receiving anticoagulation therapy or high-dose
aspirin, and for elderly patients with borderline
renal function. Timing of medication should be
adjusted to the pattern of pain (e.g. night-time
pain or pain on exercise) to obtain maximum
benet.
Local injection with corticosteroid has limited
benet, except in the presence of active inam-
mation, and should be used judiciously as
repeated steroid injection produces tissue atro-
phy which will further weaken the rotator cuff
and periarticular soft tissues in the longer term.
Test injection with local anaesthetic or T2-
weighted MRI images may help to target corti-
costeroid use to the maximum benet. By
blocking some of the sensory supply to the shoul-
der, suprascapular nerve blockade may have a
role as a pain-relieving procedure. Careful exam-
ination may reveal evidence of autonomic dis-
turbance such as colour, temperature or sweating
changes that may suggest RSD, in which case
sympathetic blockade or oral steroids may be
considered.
As an important part of any integrated care
pathway, careful assessment (if possible using
validated measures) should be repeated regularly
to monitor the treatment response. This is par-
ticularly important in HSP where the nature of
the condition is likely to change over time,
requiring appropriate modication of manage-
ment strategies. To provide effective pain relief
it is helpful to know whether pain is constant, or
worse at specic times such as at night, or during
physiotherapy. Pain assessment is particularly
difcult in the stroke population, so a battery of
simple tools accessible to people with communi-
cation, perceptual and cognitive difculties is
required to follow progress.
Acknowledgements
The authors would like to thank the John
Squire Library staff at Northwick Park Hospital
and Tabi Turner-Stokes for help with gathering
the literature. Also staff and colleagues on the
Regional Rehabilitation Unit for support and
helpful discussion. The preparation of this article
was supported nancially by an audit grant from
the North Thames Regional Audit Fund, admin-
may present with a complex mixture of underly-
ing causes, it polarizes into two distinct condi-
tions which require quite different approaches to
management. At one end is the oppy subluxed
(accid) shoulder, requiring careful support to
avoid damage to soft tissues and nerves. At the
other end of the spectrum is the stiff (spastic)
shoulder associated with soft tissue contractures
which hold the arm in a position of adduction and
internal rotation. Over time, patients may
progress from the rst towards the second. Fail-
ure to recognize these differences and their
respective requirements for management may
explain some controversies in the literature.
The accid shoulder requires particular care
in handling, even in the absence of pain. The arm
should be appropriately supported at all times,
with a wheelchair arm support by day and pillows
at night. In the preferred position the shoulder is
protracted with the arm forward, in slight abduc-
tion and neutral rotation. The wrist should be in
neutral or slight supination, and the ngers
extended, but a range of different approved posi-
tions may be determined for each patient. An
individually selected shoulder brace or sling may
offer support as the patient gets onto their feet,
as well as reminding staff of the need for care in
handling. Neurophysiotherapy techniques may be
employed to restore alignment and maintain
functional range of movement, but with care to
avoid impingement or damage to the rotator cuff.
FES may have a role to play in reducing sublux-
ation and enhancing return of muscle activity.
The spastic shoulder is likely to be more
acutely painful and may respond to analgesic or
antispasmodic medication. Positioning is impor-
tant here to try to relieve spasticity. External
rotation and abduction of the arm are to be
encouraged once spasticity in the medial rotators
of the shoulder has been reduced by properly
trained staff. Overhead exercise pulleys are to be
avoided at all costs. In resistant cases, soft tissue
release may be considered, but spasticity is often
self-limiting with appropriate treatment, and fur-
ther work is required to explore the role of less
invasive procedures such as nerve blockade or
botulinum toxin to provide localized relief of
spasticity.
A therapeutic trial of NSAIDs or simple anal-
gesia may be offered, providing there are no con-
at PENNSYLVANIA STATE UNIV on June 5, 2014 cre.sagepub.com Downloaded from
Shoulder pain after stroke 295
20 Clarke GR, Willis LA, Fish WW, Nichols PJR.
Preliminary studies in measuring range of motion
in normal and painful stiff shoulders. Rheumatol
Rehabil 1975; 14: 3946.
21 Saario L. The range of motion of the shoulder at
various ages. Acta Orthop Scand 1963; 33: 366.
22 Van der Windt DAWM, Koes BW, de Jong BA,
Bouter LM. Shoulder disorders in general practice:
incidence, patient characteristics, and management.
Ann Rheum Dis 1995; 54: 95964.
23 Pope DP, Croft PR, Pritchard CM, Silman AJ.
Prevalence of shoulder pain in the community: the
inuence of case denition. Ann Rheum Dis 1997;
56: 30812.
24 Moskowitz H, Goodman CR, Smith E, Balthazar
E, Mellins HZ. Hemiplegic shoulder. N Y State J
Med 1969; 69: 54850.
25 Johnstone M. Restoration of motor function in the
stroke patient, third edition. New York: Churchill
Livingstone, 1987.
26 Chaco J, Wolf E. Subluxation of the glenohumeral
joint in hemiplegia. Am J Phys Med 1971; 50:
13943.
27 Ryerson S, Levit K. The shoulder in hemiplegia.
In: Donatelli R ed. Physical therapy of the
shoulder, second edition. New York: Churchill
Livingstone, 1991.
28 Basmajian JV, Bazant FJ. Factors preventing
downward dislocation of the adducted shoulder
joint. J Bone Joint Surg 1959; 41: 118286.
29 Cailliet R. The shoulder in hemiplegia.
Philadelphia: FA Davies, 1980.
30 Culham EG, Noce RR, Bagg SD. Shoulder
complex position and glenohumeral subluxation in
hemiplegia. Arch Phys Med Rehabil 1995; 76:
85764.
31 Prevost R, Arsenault AB, Dutil E, Drouin G.
Rotation of the scapula and shoulder subluxation
in hemiplegia. Arch Phys Med Rehabil 1987; 68:
78690.
32 Prevost R, Arsenault AB, Dutil E, Drouin G.
Shoulder subluxation in hemiplegia: a radiologic
correlational study. Arch Phys Med Rehabil 1987;
68: 78285.
33 Najenson T, Yacubovich E, Pikielni SS. Rotator
cuff injury in shoulder joints of hemiplegic
patients. Scand J Rehabil Med 1971; 3: 13137.
34 Ring H, Leillen B, Server S, Luz Y, Solzi P.
Temporal changes in electrophysiological, clinical
and radiological parameters in the hemiplegics
shoulder. Scand J Rehabil Med 1985; 12 (suppl):
12427.
35 Lee KH, Khunadorn F. Painful shoulder in
hemiplegic patients: a study of the suprascapular
nerve. Arch Phys Med Rehabil 1986; 67: 81820.
36 Kaplan PE, Meredith J, Taft G, Betts HB. Stroke
and brachial plexus injury: a difcult problem.
Arch Phys Med Rehabil 1977; 58: 41518.
istered by Hillingdon Health Authority, and by
the Luff Foundation.
References
1 Teasell R. Musculoskeletal complications of
hemiplegia following stroke. Semin Arthritis Rheum
1991; 20: 38595.
2 Braun RM, West F, Monney V, Nickel V, Roper
B, Caldwell C. Surgical treatment of the painful
shoulder contracture in the stroke patient. J Bone
Joint Surg 1971; 53A: 130712.
3 Mulley GP. Avoidable complications of stroke. J R
Coll Physicians 1982; 16: 9497.
4 Roy CW, Sands MR, Hill LD. Shoulder pain in
acutely admitted hemiplegics. Clin Rehabil 1994; 8:
33440.
5 Roy CW, Sands MR, Hill LD, Harrison A,
Marshall S. The effect of shoulder pain on
outcome of acute hemiplegia. Clin Rehabil 1995; 9:
2127.
6 Andersen LT. Shoulder pain in hemiplegia. Am J
Occup Ther 1985; 39: 1119.
7 Forster A. The painful hemiplegic shoulder:
Physiotherapy treatment. Rev Clin Gerontol 1994;
4: 34348.
8 Grifn J, Reddin G. Shoulder pain in patients with
hemiplegia. A literature review. Phys Ther 1981;
61: 104145.
9 Grifn JW. Hemiplegic shoulder pain. Phys Ther
1986; 66: 188493.
10 Roy CW. Shoulder pain in hemiplegia. A literature
review. Clin Rehabil 1988; 2: 3544.
11 Wanklyn P. The painful hemiplegic shoulder:
pathogenesis, diagnosis and management. Rev
Clinic Gerontol 1994; 4: 24551.
12 Van Langenberghe HVK, Partridge CJ, Edwards
MS, Mee R. Shoulder pain in hemiplegia a
literature review. Physiother Pract 1988; 4: 15562.
13 Shepherd RB, Carr JH. The shoulder following
stroke: preserving musculoskeletal integrity for
function. Top Stroke Rehabil 1998; 4: 3553.
14 Turner-Stokes L. Clinical differential diagnosis of
shoulder pain. Br J Hosp Med 1996; 56: 7377.
15 Lucas DB. Biomechanics of the shoulder joint.
Arch Surg 1973; 107: 42532.
16 Constant CR. Historical background, anatomy and
shoulder function. Baillieres Clin Rheumatol 1989;
3: 42935.
17 Poppen NK, Walker PS. Normal and abnormal
motion of the shoulder. J Bone Joint Surg 1976;
58-A: 195200.
18 DePalma AF. Surgery of the shoulder.
Philadelphia: JB Lippincott, 1993.
19 Neer CS. Impingement lesions. Clin Orthop Rel
Res 1983; 173: 7077.
at PENNSYLVANIA STATE UNIV on June 5, 2014 cre.sagepub.com Downloaded from
296 L Turner-Stokes and D Jackson
54 Peszczynski M, Rardin TE. The incidence of
painful shoulder in hemiplegia. Bull Poll Med Sci
Hist 1965; 8: 2123.
55 Chang JJ, Tsau JC, Lin YT. Predictors of shoulder
subluxation in stroke patients. Kao-Hsiung i Hsueh
Ko Hsueh Tsa Chih [Kaohsiung J Med Sci] 1995;
11: 25056.
56 Ring H, Feder M, Berchadsky R, Samuels G.
Prevalence of pain and malalignment in the
hemiplegics shoulder at admission for
rehabilitation: a preventive approach. Eur J Phys
Med Rehabil 1993; 3: 199203.
57 Jensen EM. The hemiplegic shoulder. Scand J
Rehabil Med 1980; 7 (suppl): 11319.
58 Brocklehurst JC, Andrews K, Richards B, Laycock
P. How much physical therapy for patients with
stroke? BMJ 1978; 1: 130710.
59 Tobis JS. Problems in rehabilitation of the
hemiplegic patient. NY State J Med 1957; 57:
137780.
60 Bobath K. Letter to the editor. Phys Ther 1972; 52:
44445.
61 Bobath B. Adult hemiplegia: evaluation and
treatment. London: Heinemann, 1978.
62 Davies PM. Steps to follow. The comprehensive
treatment of patients with hemiplegia, second
edition. Berlin: Springer-Verlag, 2000.
63 Van Ouwenaller C, Laplace PM, Chantraine A.
Painful shoulder in hemiplegia. Arch Phys Med
Rehabil 1986; 67: 2326.
64 Pandyan AD, Johnson GR, Price CIM, Curless
RH, Barnes MP, Rodgers H. A review of the
properties and limitations of the Ashworth and
modied Ashworth scales as measures of spasticity.
Clin Rehabil 1999; 13: 37383.
65 Ikai T, Tei K, Yoshida K, Miyano S, Yonemoto K.
Evaluation and treatment of shoulder subluxation
in hemiplegia: relationship between subluxation
and pain. Am J Phys Med Rehabil 1998; 77:
42126.
66 Caldwell CB, Wilson DJ, Braun RM. Evaluation
and treatment of the upper extremity of the
hemiplegic stroke patient. Clin Orthop 1969; 63:
6993.
67 Hecht JS. Subscapular nerve block in the painful
hemiplegic shoulder. Arch Phys Med Rehabil 1992;
73: 103639.
68 Bruckner FE, Nye JS. A prospective study of
adhesive capsulitis of the shoulder (frozen
shoulder) in a high risk population. Q J Med 1981;
198: 191204.
69 Rizk TE, Christopher RP, Pinals RS, Salazar JE,
Higgins C. Arthrographic studies in painful
hemiplegic shoulders. Arch Phys Med Rehabil
1984; 65: 25456.
70 Hakuno A, Sahika H, Ohkawa T, Itoh R.
Arthrographic ndings in hemiplegic shoulders.
Arch Phys Med Rehabil 1984; 65: 70611.
37 Chino N. Electrophysiological investigation on
shoulder subluxation in hemiplegics. Scand J
Rehabil Med 1981; 13: 1721.
38 Shahani BT, Kelly EB, Glasser S. Hemiplegic
shoulder subluxation. Arch Phys Med Rehabil
1981; 62: 519.
39 Jespersen HF, Jorgensen HS, Nakayama H, Olsen
TS. Shoulder pain after a stroke. Int J Rehabil Res
1995; 18: 27376.
40 Zorowitz RD, Hughes MB, Idank D, Ikai T,
Johnston MV. Shoulder pain and subluxation after
stroke: correlation or coincidence? Am J Occup
Ther 1996; 50: 194201.
41 Bohannon RW, Larkin PA, Smith MB, Horton
MG. Shoulder pain in hemiplegia: statistical
relationship with ve variables. Arch Phys Med
Rehabil 1986; 67: 51416.
42 Bohannon RW, Andrews AW. Shoulder
subluxation and pain in stroke patients. Am J
Occup Ther 1990; 44: 507509.
43 Tepperman PS, Greyson ND, Hilbert L, Jiminez J,
Williams JI. Reex sympathetic dystrophy in
hemiplegia. Arch Phys Med Rehabil 1984; 65:
44247.
44 Cheng PT, Lee CE, Liaw MY, Wong MK, Hsueh
TC. Risk factors of hemiplegic shoulder pain in
stroke patients. J Musculoskeletal Pain 1995; 3:
5973.
45 Poulin de Courval L, Barsauskas A, Berenbaum B
et al. Painful shoulder in the hemiplegic and
unilateral neglect. Arch Phys Med Rehabil 1990;
71: 67376.
46 Wanklyn P, Forster A, Young J. Hemiplegic
shoulder pain (HSP): natural history and
investigation of associated features. Disabil Rehabil
1996; 18: 497501.
47 Parker VM, Wade DT, Langton Hewer R. Loss of
arm function after stroke: measurement, frequency
and recovery. Int Rehabil Med 1986; 8: 6973.
48 Joynt RL. The source of shoulder pain in
hemiplegia. Arch Phys Med Rehabil 1992; 73:
40913.
49 Melzack R. The McGill Pain Questionnaire. In:
Melzack R ed. Pain measurement and assessment.
New York: Raven Press, 1983: 4147.
50 Price CIM, Curless RH, Rodgers H. Can stroke
patients use visual analogue scales? Stroke 1999;
30: 135761.
51 Bohannon RW, LeFort A. Hemiplegic shoulder
pain measured with the Ritchie Articular Index.
Int J Rehabil Res 1986; 9: 37981.
52 Constant CR, Murley AH. A clinical method of
functional assessment of the shoulder. Clin Orthop
1987; 214: 16064.
53 Davis S, Petrillo CR, Eichberg RD, Chu DS.
Shoulder-hand syndrome in a hemiplegic
population: a 5-year retrospective study. Arch Phys
Med Rehabil 1977; 58: 35356.
at PENNSYLVANIA STATE UNIV on June 5, 2014 cre.sagepub.com Downloaded from
Shoulder pain after stroke 297
88 Hurd MM, Farrell KH, Waylonis GW. Shoulder
sling for hemiplegia: friend or foe? Arch Phys Med
Rehabil 1974; 55: 51922.
89 Miller J. Shoulder pain from subluxation in the
hemiplegic (Letter). BMJ 1975; 4 (5992): 345.
90 Prevost R. Bobath axillary support for adults with
hemiplegia. A biomechanical analysis. Phys Ther
1988; 68: 22832.
91 Spaulding SJ. Biomechanical analysis of four
supports for the subluxed hemiparetic shoulder.
Can J Occup Ther Rev Can dErgother 1999; 66:
16975.
92 Cool JC. Biomechanics of orthoses for the
subluxed shoulder. Prosthet Orthot Int 1989; 13:
9096.
93 Moodie NB, Brisbin J, Morgan AMG. Subluxation
of the glenohumeral joint in hemiplegia: evaluation
of supportive devices. Physiother Can 1986; 38:
15157.
94 Boyd EA, Pepin P, Szabo-Hartin J. Shoulder
supports revisited: a Canadian follow-up survey.
Can J Occup Ther Rev Can dErgother 1999; 66:
16168.
95 Zorowitz RD, Idank D, Ikai T, Hughes MB,
Johnston MV. Shoulder subluxation after stroke: a
comparison of four supports. Arch Phys Med
Rehabil 1995; 76: 76371.
96 Williams R, Taffs L, Minuk T. Evaluation of two
support methods for the subluxated shoulder of
hemiplegic patients [published erratum appears in
Phys Ther 1988 Dec; 68(12): 1969]. Phys Ther
1988; 68: 120914.
97 Ancliffe J. Strapping the shoulder in patients
following a cerebrovascular accident (CVA): a
pilot study. Aust Physiother 1992; 38: 3740.
98 Pinzur MS, Hopkins GE. Biceps tenodesis for
painful inferior subluxation of the shoulder in
adult acquired hemiplegia. Clin Orthop Rel Res
1986; 206: 100103.
99 Kumar R, Metter EJ, Mehta AJ, Chew T.
Shoulder pain in hemiplegia: The role of exercise.
Am J Phys Med Rehabil 1990; 69: 205208.
100 Savinelli R, Timm M, Montgomery J et al. Therapy
evaluation and management of patients with
hemiplegia. Clin Orthop 1978; 131: 1529.
101 Binder-Macleod SA, Lee SCK. Assessment of the
efcacy of functional electrical stimulation in
patients with hemiplegia. Top Stroke Rehabil 1997;
3: 8898.
102 Price CM, Pandyan AD. Electric stimulation for
preventing and treating post-stroke shoulder pain
(Cochrane Review). In: The Cochrane Library
1999, Issue 4. Oxford: Update Software, 199.
103 Linn SL, Granat MH, Lees KR. Prevention of
shoulder subluxation after stroke with electrical
stimulation. Stroke 1999; 30: 96368.
104 Faghri PD, Rodgers MM, Glaser RM, Bors JG,
Ho C, Akuthota P. The effects of functional
71 Van Langenberghe HVK, Hogan BM. Degree of
pain and grade of subluxation in the painful
hemiplegic shoulder. Scand J Rehabil Med 1988;
20: 16166.
72 Fitzgerald-Finch OP, Gibson IIJM. Subluxation of
the shoulder in hemiplegia. Age Ageing 1975; 4: 16.
73 Shai G, Ring H, Costeff H, Solzi P. Glenohumeral
malalignment in the hemiplegic shoulder. An early
radiologic sign. Scand J Rehabil Med 1984; 16:
13336.
74 Smith RG, Cruikshank JG, Dunbar S, Akhtar AJ.
Malalignment of the shoulder after stroke. Br Med
J Clin Res Ed 1982; 284 (6324): 122426.
75 Hall J, Dudgeon B, Guthrie M. Validity of clinical
measures of shoulder subluxation in adults with
post-stroke hemiplegia. Am J Occup Ther 1995; 49:
52633.
76 Boyd EA, Torrance GM. Clinical measures of
shoulder subluxation: their reliability. Can J Public
Health. Rev Can Sante Publique 1992; 83 (suppl 2):
S24S28.
77 Hayes KW, Sullivan JE. Reliability of a new
device used to measure shoulder subluxation. Phys
Ther 1989; 69: 79267.
78 Arsenault AB, Bilodeau M, Dutil E, Riley E.
Clinical signicance of the V-shaped space in the
subluxed shoulder of hemiplegics. Stroke 1991; 22:
86771.
79 Brooke MM, De-Lateur BJ, Diana-Rigby GC,
Questad KA. Shoulder subluxation in hemiplegia;
Effects of three different supports. Arch Phys Med
Rehabil 1991; 72: 58286.
80 Nepomuceno CS, Miller JM. Shoulder
arthrography in hemiplegic patients. Arch Phys
Med Rehabil 1974; 55: 4951.
81 Kingery WS, Date ES, Bocobo CR. The absence
of brachial plexus injury in stroke. Am J Phys Med
Rehabil 1993; 72: 12735.
82 Bhala RP. Electromyographic evidence of lower
motor neuron involvement in hemiplegia. Arch
Phys Med Rehabil 1968; 50: 63237, 641.
83 Steinbrocker O. Shoulder-hand syndrome:
association of homolateral disability of shoulder
and hand with swelling and atrophy of the hand.
Am J Med 1947; 3: 402.
84 Bonica JJ. Causalgia and other reex sympathetic
dystrophies. Postgrad Med 1973; 53: 14348.
85 Eto F, Yoshikawa M, Ueda S, Hirai S. Post-
hemiplegic shoulder-hand syndrome, with special
reference to cerebral localisation. J Am Geriatr Soc
1980; 28: 1317.
86 Dean CM, Mackey FH, Katrak P. Examination of
shoulder positioning after stroke: a randomised
controlled pilot trial. Aust J Physiother 2000; 46:
3540.
87 Carr EK, Kenney FD. Positioning of the stroke
patient: a review of the literature. Int J Nurs Stud
1992; 29: 35569.
at PENNSYLVANIA STATE UNIV on June 5, 2014 cre.sagepub.com Downloaded from
298 L Turner-Stokes and D Jackson
of interventions for painful shoulder: selection
criteria, outcome assessment and efcacy. BMJ
1998; 316: 35460.
113 Dekker JHM, Wagenaar RC, Lankhorst GJ, De
Jong BA. The painful hemiplegic shoulder: effects
of intra-articular triamcinolone acetonide. Am J
Phys Med Rehabil 1997; 76: 4348.
114 Gado K, Emery P. Modied suprascapular nerve
block with bupivacaine alone effectively controls
chronic shoulder pain in patients with rheumatoid
arthritis. Ann Rheum Dis 1993; 52: 21518.
115 Vecchio PC, Adebajo AO, Hazleman BL.
Suprascapular block for persistent rotator cuff
lesions. J Rheumatol 1993; 20: 45355.
116 Wassef MR. Suprascapular nerve block. A new
approach for the management of frozen shoulder.
Anaesthesia 1992; 47: 12024.
117 Swan DM. Shoulder-hand syndrome following
hemiplegia. Neurology 1954; 4: 48082.
118 Braus DF, Krauss JK, Strobel J. The shoulder-
hand syndrome after stroke: a prospective clinical
trial. Ann Neurol 1994; 36: 72833.
119 Geurts ACH, Visschers BAJT, van Limbeek J,
Ribbers GM. Systematic review of aetiology and
treatment of post-stroke hand oedema and
shoulder-hand syndrome. Scand J Rehabil Med
2000; 32: 410.
120 Hamamci N, Dursun E, Urai C, Cakci A.
Calcitonin treatment in reex sympathetic
dystrophy: a preliminary study. Br J Clin Pract
1996; 50: 37375.
121 Snow BJ, Tsui JKC, Bhatt MH, Varelas M,
Hashimoto SA, Calne D. Treatment of spasticity
with botulinum toxin: a double blind study. Ann
Neurol 1990; 28: 51215.
electrical stimulation on shoulder subluxation, arm
function recovery, and shoulder pain in hemiplegic
stroke patients. Arch Phys Med Rehabil 1994; 75:
7379.
105 Chantraine A, Baribeault A, Uebelhart D,
Gremion G. Shoulder pain and dysfunction in
hemiplegia: effects of functional electrical
stimulation. Arch Phys Med Rehabil 1999; 80:
32831.
106 Baker LL, Parker K. Neuromuscular electrical
stimulation of the muscles surrounding the
shoulder. Phys Ther 1986; 66: 193037.
107 Kobayashi H, Onishi H, Ihashi K, Yagi R, Handa
Y. Reduction in subluxation and improved muscle
function of the hemiplegic shoulder joint after
therapeutic electrical stimulation. J Electromyogr
Kinesiol 1999; 9: 32736.
108 Leandri M, Parodi CI, Corrieri N, Rigardo S.
Comparison of TENS treatments in hemiplegic
shoulder pain. Scand J Rehabil Med 1990; 22:
6972.
109 Prada G, Tallis R. Treatment of the neglect
syndrome in stroke patients using a contingency
electrical stimulator. Clin Rehabil 1995; 9: 30413.
110 Snels I, Beckerman H, Lankhorst GJ, Bouter LM.
Treatment of hemiplegic shoulder pain in the
Netherlands: results of a national survey. Clin
Rehabil 2000; 14: 2027.
111 Van der Windt DAWM, Van der Heijden GJMG,
Scholten RJPM, Koes BW, Bouter LM. The
efcacy of nonsteroidal anti-inammatory drugs
(NSAIDs) for shoulder complaints. A systematic
review. J Clin Epidemiol 1995; 48: 691704.
112 Green S, Buchbinder R, Glazier R, Forbes A.
Systematic review of randomised controlled trials
at PENNSYLVANIA STATE UNIV on June 5, 2014 cre.sagepub.com Downloaded from