shoulder pain after stroke

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2002 16: 276Clin RehabilLynne Turner-Stokes and Diana Jackson

an integrated care pathwayShoulder pain after stroke: a review of the evidence base to inform the development of

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Clinical Rehabilitation 2002; 16: 276–298

© Arnold 2002 10.1191/0269215502cr491oa

Address for correspondence: Lynne Turner-Stokes, RegionalRehabilitation Unit, Northwick Park Hospital, WatfordRoad, Harrow, Middlesex HA1 3UJ, UK. e-mail:[email protected]

Shoulder pain after stroke: a review of theevidence base to inform the development ofan integrated care pathwayLynne Turner-Stokes and Diana Jackson Northwick Park and St Mark’s 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 canimpede rehabilitation and has been associated with poorer outcomes andprolonged hospital stay. This systematic review was undertaken to inform thedevelopment of an evidence-based integrated care pathway (ICP) for themanagement 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 publishedstudies on shoulder pain in stroke or hemiplegia and references to literatureused in reviews (total references = 121).Main � ndings: Although a complex variety of physical changes are associatedwith HSP, these broadly divide into ‘�accid’ and ‘spastic’ presentations.Management should vary accordingly; each presentation requiring differentapproaches to handling, support and intervention. (1) In the �accid stage, theshoulder is prone to inferior subluxation and vulnerable to soft-tissue damage.The arm should be supported at all times and functional electrical stimulationmay reduce subluxation and enhance return of muscle activity. (2) In thespastic stage, movement is often severely limited. Relieving spasticity andmaintaining range requires expert handling; overhead exercise pulleys shouldnever be used. Local steroid injections should be avoided unless there is clearevidence of an in�ammatory lesion. Conclusions: HSP requires co-ordinated multidisciplinary management tominimize interference with rehabilitation and optimize outcome. Furtherresearch is needed to determine effective prophylaxis and document the

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Shoulder pain after stroke 277

Introduction

Shoulder pain is a common and distressing com-plication of stroke, interfering with both functionand quality of life.1 If the shoulder is very painfulthe patient may prefer not to move, or may with-draw from active rehabilitation.2 A protected andimmobile shoulder may interfere not only withupper limb function, but with balance, walking,transfers and performance of self-care activities.3Hemiplegic shoulder pain (HSP) can thereforeimpede the process of rehabilitation, and hasbeen associated with poorer outcomes andincreased length of stay in hospital.4,5

To address this problem, hemiplegic shoulderpain was selected as an appropriate area fordevelopment of an integrated care pathway(ICP). In keeping with the principle that the ICPshould be based on evidence, and as a prelimi-nary step in its development, a systematic reviewof the literature was undertaken. The authorswould like to stress that this review is notintended to be a Cochrane style review around alimited research question with clear exclusion cri-teria, odds ratio calculation, etc. Instead we havetaken a systematic approach to searching the rel-evant literature to assimilate current knowledgeand appraise the evidence for each aspect of clin-ical management. The aims of the review were:

1. To provide the reader with a backgroundunderstanding of the functional anatomy ofthe shoulder and how it is affected by stroke.

2. To review the literature describing frequencyand causation of HSP and the evidence forfactors contributing to its development, thusindicating potential routes to prevention.

3. To appraise the evidence for effectiveness ofdifferent interventions for HSP.

From this we have drawn conclusions on bestpractice to underpin an ICP for the multidisci-plinary management of HSP which is presentedseparately for publication.

Search strategy

Electronic literature searches were performedthrough the British Medical Association OvidOnline service using the following keywords:

1) Shoulder pain or shoulder dislocation orshoulder impingement syndrome or shoulderinjury or frozen shoulder

2) Stroke (all subheadings)3) Hemiplegia or hemiplegic.mp 4) ‘Hemiparesis’ or ‘hemiparetic’5) 2 or 3 or 46) 1 and 5.

References from EMBASE 1988–2000 (n = 63)and MEDLINE 1966–2000 (n = 44) were pooledand duplicates discarded leaving 91 references. Inaddition, relevant references listed in review arti-cles,1,6–13 but not identi�ed in the search (usuallybecause they were journals or books that werenot indexed) were obtained, giving a total of 121articles included in the review.

Functional anatomy of the shoulderand changes following a stroke

In order to understand the literature, it is help-ful to have a background understanding of thefunctional anatomy of the shoulder and how thismay be changed by a stroke.

In humans, the shoulder has evolved to pro-vide an extended range of movement in order tofacilitate hand placement for dextrous function.However, this extended range is at the expenseof 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-socketjoint 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 tomanagement of this complex condition, thus providing a sound basis forprospective evaluation of different interventions in the future.



278 L Turner-Stokes and D Jackson

2) Humeral rotation which alters the position ofthe humeral tubercles in relation to the arch.Flexion must be accompanied by medial rota-tion (subscapularis) and abduction by lateralrotation (infraspinatus) to avoid impinge-ment.18

Failure of any of these mechanisms to operateduring elevation of the arm will cause impinge-ment of supraspinatus or the long head ofbiceps.19 Repeated episodes of mechanical wearmay result in a vicious cycle of pain, in�amma-tion and the risk of further damage to the cuff bycompression or ischaemia.

Changes with ageSince 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 shoulderstructures, which are likely to represent normal-ity in that age group. Painless range of movementin the shoulder decreases with age20 as a result ofpostural change and degeneration in the articu-lar surfaces and soft tissues around the complexof joints.21 The development of dorsal kyphosismay 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 decadeof life.18 The rotator cuff thins and frays and cal-ci�c deposits may appear in the tendons. Synovialhypertrophy in the subacromial bursa and osteo-phytic change in the ACJ serve to narrow thesubacromial space and increase the likelihood ofdamage to the already weakened rotator cuff.Partial tears of the rotator cuff are common afterthe age of 50–60 years, and the most severe tearsoccur from 60 to 70 years.18 Shoulder pain is rec-ognized as a common problem among the gen-eral population, with an estimated yearlyreported incidence of 1–2.5%22,23 and with thegreatest proportion of shoulder problems beingreported during the 5th–7th decades.22

Changes following a strokeImmediately following central motor lesions,

such as stroke, there is an initial �accid paralysisin over 90% of individuals24 which is oftenreplaced by a predictable pattern of spasticity ina timescale which may vary from 24 hours24 to12–18 months25–27 Alteration in the alignment of

enlarged by the cartilaginous glenoid labrumwhich enhances stability without restrictingmovement.15 The role of the rotator cuff musclesis to ‘tuck in’ the humeral head to form a stablefulcrum for elevation.16 An important function ofthis tucking-in is that the humeral head is low-ered away from the acromion. If rotator cufffunction 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 ofthe supraspinatus tendon between the humeralhead and the acromion (Figure 1).

In addition to this ‘tucking-in’ function, twoother 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 theglenoid to maintain a position of �rm oppo-sition to the humeral head.15 Scapular rota-tion is principally controlled by the trapeziusand serratus anterior muscles.15

Figure 1 Shoulder structures and impingement of thesupraspinatus tendon.




skeletal components of the shoulder complexhave been described in both the �accid and spas-tic stages of paralysis after stroke, and each hasbeen implicated in the causation of HSP.

In �accid paralysis of the shoulder, weaknessin the shoulder girdle muscles and gravitationalpull tend to result in inferior subluxation,although the exact mechanism for this remainsthe subject of debate.28–32 In addition, weaknessin the muscles that effect scapular and humeralrotation during elevation results in failure of themechanisms that normally protect againstimpingement. The danger of rotator cuff damageduring passive elevation of the arm is thereforeincreased.33 The weight of the unsupported armmay also cause traction damage to various nervesincluding the axillary nerve,34 the suprascapularnerve35 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 thesupraspinatus muscles may reduce inferior sub-luxation,26 but now the scapular rotation may beimpeded by increased tone in the latissimus dorsi,levator scapulae and rhomboid muscles.29 Fur-thermore, activity in the medial rotators may pullthe humerus into internal rotation, thus con-tributing to impingement on active and passiveGHJ abduction. The humeral head may now beanteriorly displaced. However, if inferior sublux-ation was severe during the �accid stage, it mayremain inferiorly displaced due to permanentstretching or damage to the rotator cuff.33,38

Increased muscle tone may cause pain by pro-ducing sustained traction on periosteal muscleattachments, which are rich in sensory receptors.2

Such spasticity interferes with normal scapulo-humeral movement and increases the likelihoodof contractures.8 Once contractures have devel-oped, attempts to stretch the contracture causepain, generating re�ex protective spasm andpatient apprehension. There is consequently avicious cycle of reduced movement, increasingrestriction with disuse atrophy and osteoporosisoccurring as late events.29

In summary, it appears that deranged anatomyin both �accid and spastic stages may contributeto HSP, although the mechanisms are different.In the next section we review the evidence forthese mechanisms in greater detail. It will be seen

that the evidence is confounded by the fact thatmany patients go through both stages and, unfor-tunately, the relative incidence of spasticity and�accidity to HSP in the literature are not welldocumented.8 On top of either condition, soft-tis-sue damage resulting from improper handlingpresents a further confounding factor.8,9,12

Incidence and causation of HSP andthe evidence for factors contributingto its development

Reports of frequency of shoulder pain in the lit-erature vary between 5 and 84% and are listedin Table 1. There are a number of reasons for thisvariation. Many of the studies are retrospectiveand so must be regarded with caution. The �g-ures are also dif�cult to compare, as many of thepopulations are selected and it is not always clearwhether incidence or prevalence is beingreported.12 Most of the epidemiological data havebeen gathered from patients attending rehabili-tation programmes, so the incidence of HSP isunknown in patients not attending for rehabilita-tion, those with mild disability only, or those whohave been discharged from treatment.9

Pain is not consistently described. Some stud-ies appear to be reporting pain which occursspontaneously,4,33,39,40 but some report only painon passive movement.41,42 Others include eithertype of pain2,34,43 and only a few studies make aclear distinction between them.44–47 If pain is cat-egorized by severity, mild pain may be includedeither with the ‘no pain’48 or the ‘some pain’41

category.Pain is a subjective symptom which is dif�cult

to measure even in patients with intact sensori-motor, cognitive and communication facilities.Standard pain assessment techniques such asvisual analogue scales may be inappropriate forpatients with visuospatial neglect, and self-com-pleted questionnaires, such as the McGill PainScore49 may be inaccessible for patients withaphasia. Price et al. have demonstrated thatstroke patients as a group form poor witnessesfor many types of visual analogue scale.50

Bohnannon and Andrews used the Ritchie indexto measure shoulder pain in stroke patients51 andreliability testing suggests that agreement using




demonstrated an association.40,41,44

As will be shown later in this review, withinthe group of patients with substantial upper limbde�cits, it is likely that other factors such as softtissue damage or spasticity may intervene to havea greater effect on pain, than severity of thestroke de�cit per se.

Time after stroke is also a factor. As alreadydescribed, the natural progression of hemiplegiaover time is characterized by changes in muscletone, weakness and loss of normal range ofmovement. All these have an effect on normalshoulder posture and render the shoulder vul-nerable to contractures and soft tissue damagefrom inappropriate handling. It is not surprising,therefore, to �nd that the likelihood of develop-ing HSP increases over time. Prospective studiesreport HSP starting almost immediately afterstroke in a few patients, with the majority devel-oping pain some weeks or months later.4,46 In onelongitudinal study,58 pain and stiffness werefound to be present in 16% of their 135 patientsat two weeks post stroke, but by one year anadditional 27% complained of pain. Bohannon etal.41 showed an inter-relationship between timesince stroke, range of shoulder external rotationand severity of shoulder pain.

this method of rating is substantial.42 Assess-ments based on shoulder function52 are unsuit-able in the nonfunctional upper limb. There is asyet no well-validated instrument speci�callydeveloped for de�ning shoulder pain in strokepatients.

Most studies agree that HSP is independent ofage and sex.9,44 Reports vary with regard to sideof stroke, and some have found no relationshipat all.44 On the other hand, it has been postulatedthat patients with neglect, due to right hemi-sphere damage, may not protect their paralysedupper limb effectively and therefore be at greaterrisk of trauma. Poulin de Courval et al.45 foundthat pain was signi�cantly more common in lefthemiplegics, but there was no relationshipbetween pain and the presence of left hemi-neglect. By contrast, other studies have found apreponderance of right hemiplegia in associationwith HSP.53,54

Many authors concur that the incidence of painis related to severity of paresis.4,55,56 In a group ofpatients with severe paralysis,33 84% of patientshad moderate or severe shoulder pain. Patientswith slight paresis only rarely complain of shoul-der pain,57 and the reference reporting thelowest incidence of HSP was a community-basedstudy47 in which 26% of patients had no armweakness. 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 197133 32 27 (84%)Braun 19712 100 70 (70%)Hurd 197488 14 8 (57%)Brocklehurst 197858 107 73 (43%)Tepperman 198443 85 17 (21%)Van Oewenaller 198663 219 157 (72%)Parker 198647 187 9 (5%)Bohannon 198641 50 36 (72%)Bohannon 199042 24 17 (70%)Poulin de Courval 199045 94 45 (48%)Ring 199356 80 43 (53%)Roy 19944 76 55 (72%)Cheng 199544 50 32 (64%)Jesperson 199539 173 38 (22%)Zorowitz 199640 20 9 (45%)Wanklyn 199611 108 69 (64%)

Range = 5–84%Mean = 54%

HSP, hemiplegic shoulder pain.




resistance to passive stretch may result fromother factors, such as the viscoelastic propertiesof soft tissues, and indeed, resistance to move-ment may be more marked in the presence ofpain.64 In addition, tone patterns can vary withinthe same hemiplegic arm, such that there is �ac-cidity around the shoulder and spasticity distally,or vice versa. They may also vary from day today.4 None of the authors make a clear distinc-tion between the presence of spasticity speci�-cally in the shoulder girdle muscles, as opposedto more generally in the upper limb. A positiveassociation between pain and spasticity wasfound in three studies.38,45,63 Shahani et al.38

reported an association between degree of painand degree of spasticity, but their study onlyincluded 10 patients. In the much larger study byVan Ouwellaner et al.63 of 219 patients there wasa particularly strong association between painand spasticity: 85% of patients with spasticityaround 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 �accidityTobis59 describes the typical picture of HSP as

�accid paralysis, atrophic shoulder musculatureand inferior subluxation. However, Bobathclaims that shoulder pain only becomes a prob-lem when spasticity develops.60,61 Physiothera-peutic reviews9,12 in particular have drawnattention to the role of spasticity in shoulderpain, because of the different therapeutic strate-gies employed to manage it.62 Table 2 summa-rizes the papers that describe the relationshipbetween HSP, spasticity and limitation of exter-nal rotation.

Spasticity is de�ned as a velocity-dependentresistance to passive stretch1 but not many stud-ies have speci�cally separated spastic and �accidshoulder pain in their analysis, nor is thereagreement on how spasticity is assessed. Moststudies simply state that tone wasassessed,41,44,48,56 but some authors assessed spas-ticity on the basis of an increased myotatic(stretch) re�ex,63 and others used the Ashworthscale.4 Doubt has been cast on the Ashworthscale 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 toin series assessed related to reduced range of

spasticity external rotation

Van Ouwenaller 198663 219 Yes Myotatic re�ex Yes Not mentioned

Bohannon 198641 50 Yes ‘Simultaneously with range during No Yesexternal rotation’

Poulin de Courval 94 Yes Physiotherapy assessment of Yes Yes199045 muscle tone:

Flaccid = 0 Normal = 1Spasticity: 2 = mild, 3 = moderate,4 = severe

Joynt 199248 67 Yes Resistance to rapid stretch No Yes

Ring 199356 80 Yes Clinical assessment Trend, Not mentionedNormal tone, hypotonic, hypertonic but N/S

Roy 19944 83 Yes Tone in shoulder rotators, elbow No Yes�exors, wrist �exors and extensors:on Ashworth Scale

Cheng 199544 50 Yes ‘Increased tone and stretch re�exes’ No Yes

Zorowitz 199595 20 No – – Yes

Wanklyn 199646 108 No – – Yes

Ikai 199865 75 No – – Yes

HSP, hemiplegic shoulder pain. at PENNSYLVANIA STATE UNIV on June 5, 2014cre.sagepub.comDownloaded from



per se.41,44,48,56 However, it can be dif�cult to dis-tinguish between active spasticity and capsularadhesion/contracture – both of which typicallyresult in a reduced range of external rotation inthe shoulder – and a number of studies havedemonstrated a strong relationship between HSPand 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 atthe muscle insertion. They reported relief of painin their series where muscular contracture wassurgically released but the capsular contractureleft intact.2 To eliminate internal rotation andadduction the subscapularis and pectoralis ten-dons were transected in an initial series of 13patients who presented with pain, limitation ofmovement and spasticity.66 Marked pain reduc-tion and increase in range of movement wereobserved in 10 patients. A follow-up study of 50patients showed similar improvement in 88%.2 Astudy by Hecht67 showed that similar resultscould be obtained by phenolization of the nervesto the subscapularis muscle, and together thesestudies suggest that active spasticity at least playsa part in the genesis of HSP.

Intracapsular in�ammation: adhesive capsulitisor ‘frozen shoulder’

Hemiplegia has been associated with the devel-opment of adhesive capsulitis41,65,68–70 and Table3 summarizes the relationship between HSP andsoft tissue lesions, which include adhesive cap-sulitis and rotator cuff tears.

Bruckner and Nye68 report ‘adhesive capsulitis’in 25% of their series of 91 patients, most ofwhom had undergone neurosurgery for sub-arachnoid haemorrhage, but they use this termloosely to describe the clinical presentation of apainful stiff shoulder from any cause. As seenabove, this picture could equally arise from spas-ticity. On the other hand, prolonged immobiliza-tion as a result of paralysis can also result insecondary capsular contracture. In the series byIkai et al.,65 23 patients had arthrograms of which74% had a small capsular outline, which he inter-preted as adhesive capsulitis, and there was amarked correlation between severity of pain and

loss of external rotation. Rizk et al.69 reported a77% incidence of adhesive capsulitis in theirarthrographic series of 30, and likewise Hakunoet al. noted a 55% incidence of adhesive changes,although there was also a 33% incidence on theunaffected side.70

In the literature on hemiplegia, adhesive cap-sulitis has been related to paralysis, unconscious-ness, impingement and subluxation.9 It is likelyalso that it is a late sequel of chronic spasticitybut, given the failure in many studies to distin-guish between active spasticity and capsular con-tracture, it is once again hard to separate causeand effect. On the basis of the above studies itseems likely that spasticity plays a signi�cant rolein the pathogenesis of shoulder pain, even thoughits effect may be obscured by subsequent con-tracture and adhesions. Therapeutic interventiontargeted towards the reduction of spasticity in itsearly stages, may therefore be an important fac-tor in reducing HSP as well as maintaining jointrange in the anticipation of future functionalrecovery.

SubluxationIn 1957, Tobis59 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 relationship4,33,56,63 and others disputingit.2,40,42,44,46,48,61,62,71 Those that present �gures aresummarized in Table 4.

Once again, confusion arises from failure tode�ne ‘subluxation’. Most commonly, the term‘subluxation’ is used to imply inferior subluxa-tion.24,42,44,46,48,71,72 The term ‘malalignment’4 orpre-subluxation73 is used by some to imply minordegrees of incongruency and ‘subluxation’ amore 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 humeralhead may be displaced anteriorly, posteriorly orin medial rotation. The direction of malalignmentis by no means always clear. Some use ‘malalign-ment’ as a general term to mean displacement in




Tab

le 3

Hem

iple

gic

pain

and

sof

t-tis

sue

lesi

ons

Aut

hor,

Met

hod

ofIn

cide

nce

ofR

elat

ions

hip

ofIn

cide

nce

ofR

elat

ions

hip

ofS

ublu

xatio

nye

aras

sess

men

tad

hesi

veca

psul

itis

to H

SP

rota

tor

cuff

RC

tea

rs t

o H

SP

(No.

sub

ject

s)ca

psul

itis

(RC

) te

ars

Naj

enso

nA

rthr

ogra

phy

Not

–13

(40

%)

All

tear

s ha

d pa

inTo

tal

inci

denc

e: 8

1%19

7133

Aff

ecte

d si

de o

nly

men

tione

d(1

0/11

pts

with

All

tear

s ha

d se

vere

(n=

32)

seve

re p

ain

in t

his

mal

alig

nmen

tse

ries

had

RC

tea

rs)

Nep

omuc

eno

Art

hrog

raph

y0

–7

(30%

)A

ll te

ars

had

pain

Tota

l in

cide

nce:

46%

1974

80A

ffec

ted

side

onl

y5/

7 (7

1%)

tear

s ha

d(n

= 2

4)su

blux

atio

n

Bru

ckne

rC

linic

al23

(25

%)

Can

not

com

pute

Not

men

tione

d–

No

data

giv

en19

8168

(Pai

nful

stif

f(D

iagn

osis

mad

e on

(n=

99)

shou

lder

)th

e ba

sis

of p

ain)

Riz

kA

rthr

ogra

phy

23 (

77%

)C

anno

t co

mpu

teN

one

–To

tal

inci

denc

e: 0

%19

8469

Aff

ecte

d si

de o

nly

(Pat

ient

s se

lect

ed o

n(n

= 3

0)th

e ba

sis

of p

ainf

ulst

iff s

houl

der)

Hak

uno

Art

hrog

raph

y42

(55

%)

Not

sig

ni�c

ant

17 (

22%

)N

ot s

igni

�can

tTo

tal

inci

denc

e 39

%19

8470

Bot

h si

des

affe

cted

sid

eaf

fect

ed s

ide

Sig

ni�c

ant

No

data

giv

en o

n(n

= 7

7)25

(33

%)

19 (

25%

)co

rrel

atio

n on

ly w

ithre

latio

nshi

p of

tea

rs o

rno

n-af

fect

edno

n-af

fect

edpa

in b

efor

e st

roke

caps

uliti

s w

ithsu

blux

atio

n

Ikai

Art

hrog

raph

y17

(74

%)

Cor

rela

tion

with

1 (4

%)

–N

o da

ta g

iven

1998

65A

ffec

ted

side

onl

ypa

in s

ever

ity a

ndFo

r th

e su

bgro

up (

23/7

5)(n

= 2

3)re

duce

d ra

nge

ofw

ho h

ad a

rthr

ogra

phy

exte

rnal

rot

atio

n

HS

P,

hem

iple

gic

shou

lder

pai

n.




other causes of shoulder pain in the various studypopulations. In studies which formally assessedthe relationship of HSP with multiple variables,there was a stronger relationship with spasticity63

and with reduced range of external rotation thanwith inferior subluxation.40,41,44,65 Even though

any direction,56 others use ‘subluxation’ for thispurpose.30,40,65 To confuse matters further, somemeasured subluxation radiologically and somejust by clinical assessment (see Table 4).

One of the reasons for a variable relationshipwith 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 Relationshipseries % subluxation to HSP

Najenson 197133 32 26 (81%) Radiological: AP radiograph Supine and erect YesInferior subluxation onlyGraded: I = subluxation,II = luxation

Fitzgerald-Finch 100 17 (17%) Radiological: AP radiograph Erect in standing –197572 Inferior subluxation only: (Patients had to

Present or absent be able to stand)

Smith 198274 110 51 (46%) Radiological: AP radiograph Supine and erect –Inferior subluxation onlyGraded: 0–3

Van Oewenaller 219 109 (50%) Radiological: AP radiograph Not speci�ed Yes198663 Inferior subluxation only:

Present or absent

Van Langenberghe 44 24 (54%) Radiological: AP radiograph Not speci�ed No198812 Inferior subluxation only

Graded: 0–4

Bohannon 199042 24 9 (37%) Clinical: Sitting (erect) NoInferior subluxation onlyGraded: 0, 1(minimal),2(substantial)

Joynt 199248 67 21 (31%) Clinical Not speci�ed NoUnspeci�ed method

Ring 199356 80 45 (56%) Radiological: AP radiograph Sitting (erect) YesInferior subluxation only: Present or absent

Cheng 199544 50 23 (46%) Clinical:Inferior subluxation only Not speci�ed YesPresent or absent

Roy 19944 76 26 (34%) Radiological: AP radiograph ‘Unsupported arm’ YesInferior subluxation only (presumed sitting)Graded: 0–4

Zorowitz 199595 20 Correlation Radiological: AP radiograph Sitting Noreported rather Subluxation in two dimensions:than incidence vertical and horizontal disparity

compared with normal side

Wanklyn 199646 108 13 (29%) Clinical: Sitting NoInferior subluxation onlyGraded in �nger-breadths

Ikai 199865 75 Selected for Radiological: AP radiograph Sitting Nosubluxation Subluxation in two dimensions:

as per Zorowitz 1995




tunately, none of the reports describing the inci-dence of subluxation and its relationship to HSPused these techniques. Although Zorowitz et al.40

refer to the methods described by Prevost,32 theyactually use the simpler two-dimensional methoddescribed 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 becomesfeasible are probably the mainstays for routineassessment of subluxation.

Extracapsular in�ammation: rotator cuff tearsAs has already been discussed under ‘func-

tional anatomy’, �exion and abduction of theshoulder must be accompanied by appropriaterotation of the scapula and humeral head toavoid impingement of the rotator cuff. The nor-mal mechanisms that protect the rotator cuff arelost in hemiplegia, and given that this group ofpatients is also likely to have degenerativechanges predisposing to rotator cuff rupture, onemay suppose that trauma due to traction on lift-ing and handling would be likely to damage therotator cuff and result in shoulder pain.57 Theproblem with relating cause and effect, however,is the relatively high incidence of asymptomatictears in this population. Papers reporting a rela-tionship between rotator cuff tears and shoulderpain are summarized in Table 3.

Joynt48 attempted to de�ne the source of HSPby injecting 1% lignocaine into various sites inthe shoulder complex. Moderate or marked reliefwas obtained by injection of the subacromialbursa in about half of his 28 patients, suggestingthat subacromial pathology makes a signi�cantcontribution to HSP at least in a proportion ofcases.

Najenson et al.33 concluded from arthrographicstudies on 32 patients that rotator cuff tearswere more common on the affected than the non-affected side. They found rotator cuff tears in40% of their patients, which were accompaniedin all cases by severe malalignment and pain.Nepomuceno and Miller similarly found rotatorcuff tears in 30% of their group of 24 patients.80

However, Hakuno et al. found no signi�cant dif-ference between the affected and nonaffectedside in his series of 77,70 Rizk et al. found norotator cuff lesions at all among their series of

one might expect the development of spasticityto reduce subluxation, the evidence suggests thatit may become irreversible after a period, per-sisting even after voluntary control or spasticityhave developed.33 This may be due to over-stretching of the capsule, ligaments andsupraspinatus and deltoid muscles38 or rupture ofthe rotator cuff33,73 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 iscomplicated by soft tissue damage, the associa-tion with pain and limitation of movement maybe higher.

The rather confused picture of subluxation inrelation to HSP con�rms the need for accurateassessment. A number of clinical methods ofassessing subluxation have been proposed, andinclude measuring arm-length discrepancy,75

assessment of the subacromial space by palpationor calipers76 or the use of a thermoplastic jig.77

Of these methods, palpation proves the most reli-able,75,76 but caliper measurement may be moresensitive and also gives reliable results.76 Theonly method which gave unacceptable reliabilitywas the jig.75,76

Shoulder subluxation may be missed radiolog-ically unless the subject is X-rayed in the erectposition.24,74 This is often dif�cult to achieve inthe earlier stages of stroke recovery. Shai et al.73

report the appearance of a V-shaped spacebetween the humeral head and glenoid fossa ona plain X-ray, as an early sign of subluxation.This is con�rmed by Arsenault et al.78 to precedethe onset of pain, and may therefore offerthe opportunity for early diagnosis and interven-tion before subluxation progress to soft tissuedamage.

Radiographic measurement offers the oppor-tunity for more detailed assessment. Prevost etal.32 describes a three-dimensional X-ray tech-nique which employs a mathematical formula totwo X-rays (one taken at 0° anterio-posterior,and the other at 45° oblique). This showed a highlevel of repeatability and correlated well withclinical tests. More recently Boyd and Torrance76

have advocated the use of a digitizer and com-puter to quantify measurements from a single X-ray, although this requires specialized equipmentto standardize the position of the patient. Unfor-




pain in hemiplegia may result from entrapmentof the suprascapular nerve. This nerve arisesfrom the upper trunk of the brachial plexus andcourses down posteriorly, passing through thesuprascapular notch before dividing into sensorybranches, supplying the acromioclavicular andglenohumeral joints, and motor branches supply-ing the supraspinatus and infraspinatus muscles.It is potentially vulnerable to entrapment at thesuprascapular notch, and it was suggested thattraction on the nerve might result frommalalignment of the scapula leading to HSP.However, only three of their 30 patients hadincreased latency on EMG on the affected sideand suprascapular nerve block did not com-pletely relieve their pain, so it was concluded thatsuprascapular entrapment was not a signi�cantcause of shoulder pain. Nevertheless, the supras-capular nerve provides some of the sensory sup-ply to the shoulder and blockade may offer thepossibility of pain relief in some cases.

An alternative explanation for lower motorneuron involvement offered by Bhala82 manyyears earlier may be pertinent – namely the con-cept of upper and lower motor neuron depen-dence and the notion that lower motor neurondegeneration may follow as a direct consequenceof a destructive lesion of the upper motorneuron.

Autonomic dysfunction: re�ex sympatheticdystrophy (RSD)

Re�ex sympathetic dystrophy (RSD) or ‘shoul-der–hand syndrome’83 is also cited as a cause ofshoulder pain in stroke, occurring in 12.5% of apopulation of 540 in a �ve-year retrospectivestudy reported by Davis et al.53 and in 28% of 219patients in Van Ouwenaller’s study.63

RSD usually appears within three months andrarely later than �ve months following stroke.53

Clinical criteria for diagnosis include severe pain,hyperaesthesia, vasomotor disturbance, oedemaand eventually atrophy in the skin and muscle ofthe shoulder and hand. There is frequently painand limitation at the shoulder, wrist andmetacarpo-phalangeal joints, while the elbow isspared.53

The mechanism of autonomic dysfunction instroke is unknown. Some have postulated peri-pheral triggers such as immobility and decreased

30,69 and Ikai et al. found only one.65

Tobis59 considered that the traction forces inGHJ subluxation contributed to rotator cufftears. It is possible that the capsular adhesionsand/or spasticity provide relative protectionagainst rotator cuff damage to which �accid sub-luxed shoulders are more prone, and the expla-nation for these different results lies in thedifferent selected populations. Najenson et al.33

recruited patients with ‘severe paralysis’ and an84% prevalence of subluxation, while Rizk et al.69

speci�cally selected patients with spasticityresulting in a painful stiff shoulder. Three-quar-ters of Ikai’s group had capsular restriction,65

while Hakuno et al.,70 appeared to have a moreequal mixture of subluxation and ‘adhesive cap-sulitis’.

It should be noted that all these studies wereundertaken using arthrography, before the era ofMRI, and the question should now be re-addressed in larger numbers, in the light of moreadvanced 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 ofpain and subluxation in the hemiplegic shoul-der.36,37 Chino reported neuropathic responses inthe supraspinatus and deltoid muscles in 75% ofhis hemiplegic population.37 Once again, causeand effect is unclear. It has been suggested thata combination of �accidity and trauma due tocareless handling are responsible for tractioninjury to the brachial plexus36 which may thenserve to enhance the subluxation.

Kingery and colleagues,81 on the other hand,cast doubt on the occurrence of brachial plexuslesions in stroke as they failed to �nd evidenceof the condition in their prospective study of 50patients. They do not report, however, how manyof these had subluxation and their series is small.It may serve only to indicate that the combina-tion of subluxation and trauma suf�cient to causethis complication are fortunately relativelyuncommon.

Ring et al. suggested that downward subluxa-tion may produce traction on the axillary nerveas it winds round the surgical neck of the humeralshaft.56

Lee and Khunadorn35 suggested that shoulder at PENNSYLVANIA STATE UNIV on June 5, 2014cre.sagepub.comDownloaded from



produce any data or references to substantiatethis statement. A recent pilot RCT86 failed toshow bene�t from a shoulder positioning proto-col but the numbers (n = 23) were too small tobe conclusive.

There is, however, some circumstantial evi-dence. Wanklyn et al. reported that the preva-lence of HSP increases during the �rst few weeksfollowing discharge from hospital.46 In that study,development of shoulder pain was more commonin patients who needed help for transfers, andnine carers admitted pulling on the hemiplegicarm, 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 differencescould not be accounted for by other factors suchas age, long waiting periods, etc., and so wereattributed to poor handling techniques.

So while there is no irrefutable evidence thatpoor handling and incorrect positioning results inincreased likelihood of HSP, the weight of pro-fessional opinion is such that a controlled trial of‘best practice’ against ‘worst practice’ would beunethical. The question, therefore, is not whetherbest practice should be applied, but what exactlyis considered to be best practice?

Carr and Kenney87 explored recommendationsin the literature for positioning in both lying andsitting. There was general concurrence that theshoulder should be protracted (to avoid retrac-tion), the arm forward, the wrist in neutral orslight supination, and the �ngers extended. Opin-ion was divided on whether the elbow should be�exed or extended, and whether the arm shouldbe abducted and externally rotated or not. Theirarticle provides an admirably systematic reviewof prevailing opinion, but fails to recognize theneed for all of us to change position from timeto time, and thus the need for a range of‘approved’ changes within each overall positionas is recommended by others.13

Static positioning is all very well when thepatient is, so to speak, a captive audience, but asthey improve and get up on their feet, the pull ofgravity puts a further vertical load on the �accidshoulder and the need for more mobile supportmust be considered.

sensory input causing an imbalance in centralneural control of the sympathetic system.84 Oth-ers have suggested that the central lesion itselfmay be responsible.85 A plain radiograph mayshow patchy demineralization, but the most spe-ci�c diagnostic test is a technetium diphos-phonate bone scan, which shows increasedperi-articular uptake, particularly at the shoulderand wrist.1

Tepperman et al.43 found evidence of RSD onbone scan in 21/85 (25%) of hemiplegic patients,although only two-thirds went on to develop theclinical syndrome. This suggests that many fea-tures associated with RSD, such as oedema, wast-ing and �exural contracture may be secondaryfeatures associated with immobility and mightexplain the confusion in the literature betweenRSD and ‘shoulder–hand’ syndrome. In this con-text, therefore, criteria for the diagnosis of RSDshould include vasomotor changes such aschanges in skin colour, temperature and sweat-ing, and MCP tenderness. Under this stricter def-inition, it is probably less common than theliterature suggests. Nevertheless, its importancelies in the fact that speci�c intervention targetedat the sympathetic nervous system may becomeappropriate if the diagnosis is con�rmed.

The evidence for effectiveness ofdifferent interventions in themanagement of HSP

Because of the diverse and multifactorial aetiol-ogy of HSP, management is often dif�cult and theresult of treatment unsatisfactory. In this last sec-tion we review the evidence for effectiveness ofdifferent interventions in the management ofHSP.

Positioning and handlingMany authors have suggested that trauma to

the shoulder joint can be prevented by properpositioning and handling.3,24,29,33,56,57,61,62,72 How-ever, much of this comment is speculative – onlyrotator cuff tears have been subjected to formalreview as evidence for this statement.12

Moskowitz et al.24 report that with proper posi-tioning and handling the incidence of HSP can bereduced from 75% to as low as 5%, but do not




tant subluxation. In general, arm slings appear toprovide the best correction of subluxation, bothin vertical79,93 and horizontal79 planes. They mayalso prevent the �accid arm from banging againstthe body during functional activities27 and be use-ful as a temporary support during early gait re-education.93,94 However, many authors expressreservations about the long-term use of slingswhich immobilize the arm in �exion, adductionand internal rotation.

Axillary supports such as the Bobath sling orroll,79,90,93,95,96 consist of a covered foam roll posi-tioned in the axilla and anchored with straps overthe shoulders or around the body. The design isdiscreet and does not encourage �exor posturingor limit movement of the arm. Originallyintended for use by patients with adductor spas-ticity,93 the axillary roll has since been evaluatedas a support for the subluxed humerus, but unfor-tunately with poor results. Not only does it failto correct subluxation to an acceptabledegree,79,90,93,95,96 it also produces lateral displace-ment of the humeral head79,95 thus increasingstress on soft tissues.90 Increasing recognition ofthis problem has probably been one of the mainreasons for the decline in popularity of the axil-lary roll over recent years.94

Humeral cuff supports attempt to emulate thedeltoid muscle by pulling the humeral head upfrom above. They consist of an adjustable cuffaround the upper part of the affected arm heldin place by a �gure of eight body harness as inthe Roylan type27,95 or a bilateral cuff joined bya yoke across the back as in the Hook hemi-har-ness.93 Zorowitz et al. found the Roylan slingallowed slight external rotation of the shoulderwhen optimally applied and it provided the besttotal reduction in subluxation.95 This type of sup-port was felt to be most appropriate for patientswith some volitional movement. In contrast, theHook hemi-harness was ineffective, restrictive tomovement and uncomfortable to wear.93

Evidence suggests, therefore, that differentsupports suit individuals at different stages inrecovery making careful evaluation essential tooptimize function of the affected limb and reducesubluxation.95 However, no study to date has for-mally addressed the reliability of everyday appli-cation by ward staff or carers. Simplicity inapplication may be as important as the intrinsic

Slings and supportsSlings and supports are frequently used in the

management of a hemiplegic patient to reducesubluxation and protect the arm from trauma.However, their use remains controversial. Notonly are they sometimes ineffective,88 they canalso reduce upper limb mobility and sensoryinput, encourage �exor tone, and impair gait andbody image.7 Slings are often applied incorrectlyor discarded by patients.89 For these reasons, it isimportant not only to consider what con�gura-tion provides the best arm position, but also whois going to put it on and whether it will actuallybe worn.6

A number of studies have explored the bio-mechanical effects of different slings90–92 with aview to helping therapists to identify thepatient’s particular condition and the sling whichmight be most appropriate. Others have madedirect radiographic comparisons of the effects ofdifferent types of sling in the same patients, butonly one group93 suggest an acceptable level forcorrection of inferior subluxation as within 0.5cm of the normal (unaffected) side. The detailsof these studies are listed in Table 5.

For chair-bound patients, an arm trough or laptray can provide support for a �accid arm andeffective reduction of subluxation,79,93 while posi-tioning the arm away from the body, discourag-ing adduction and internal rotation79 andallowing bilateral upper limb activities.93 Theirdownside is a tendency to over-correct subluxa-tion,79,93 especially if the patient slips down in thechair,91 though careful choice of seating and reg-ular monitoring of patients should overcome thisproblem.94 Both demonstrate a lesser tendency towander than the ordinary pillow. An arm troughis more likely to permit independent transfersthan a lap tray, but naturally, both become inef-fective as soon as the patient starts to spend sig-ni�cant periods of time on their feet and out oftheir chair.

Worn support devices broadly divide into threetypes: arm slings, axillary supports and humeralcuff supports. Arm slings may have contralat-eral95 or bilateral79 supporting shoulder straps butthe rationale for both types is the same, being tosupport the forearm and distribute its weight toone or both shoulders, thus preventing or reduc-ing stretch to the shoulder capsule and any resul-




Tab

le 5

Slin

gs a

nd s

uppo

rts

in t

he m

anag

emen

t of

sub

luxa

tion

Aut

hor,

yea

rA

sses

smen

tD

evic

es u

sed

Cor

rect

ion

of s

ublu

xatio

nO

vera

ll co

nclu

sion

No.

of

subj

ects

met

hods

Mea

n di

ffer

ence

fro

mun

affe

cted

arm

(cm

)

Moo

die

1986

93A

P r

adio

grap

hTr

iang

ular

ban

dage

–0.0

2 (v

ertic

al)

Eff

ectiv

e (b

ut i

mm

obili

zed

the

arm

)(n

= 1

0)In

ferio

r su

blux

atio

non

lyB

obat

h ro

ll0.

64 (

vert

ical

)In

effe

ctiv

e (u

nder

corr

ecte

d)H

ook

hem

i-har

ness

0.98

(ve

rtic

al)

Inef

fect

ive

(und

erco

rrec

ted)

Lap-

tray

–0.1

6 (v

ertic

al)

Eff

ectiv

e (b

ut o

verc

orre

cted

in

som

e ca

ses)

Arm

tro

ugh

0.07

(ve

rtic

al)

Eff

ectiv

e (b

ut o

verc

orre

cted

in

som

e ca

ses)

Will

iam

s 19

8896

AP

rad

iogr

aph

Bob

ath

roll

0.82

(ve

rtic

al)

Bet

ter

than

no

supp

ort.

Com

fort

able

to

wea

r(n

= 2

6)In

ferio

r su

blux

atio

non

lyH

ende

rson

slin

g0.

88 (

vert

ical

)B

ette

r th

an n

o su

ppor

t. C

omfo

rtab

le t

o w

ear

Zoro

witz

199

595A

P r

adio

grap

hS

ingl

e st

rap

hem

i-slin

g0.

34 (

vert

ical

)E

ffec

tive

in v

ertic

al a

nd h

oriz

onta

l pl

anes

.(n

= 2

0)V

ertic

al a

nd0.

00 (

horiz

onta

l)B

est

vert

ical

cor

rect

ion

in 5

5% o

f pa

tient

sho

rizon

tal

Bob

ath

roll

0.62

(ve

rtic

alIn

effe

ctiv

e (la

tera

l di

spla

cem

ent

of h

umer

al h

ead)

disp

lace

men

t.0.

49 (

horiz

onta

l)B

est

vert

ical

cor

rect

ion

in 2

0% o

f pa

tient

sA

lso

calc

ulat

edR

oyla

n hu

mer

al c

uff

slin

g0.

58 (

vert

ical

)E

ffec

tive

(bes

t re

duct

ion

in t

otal

ass

ymet

ry)

tota

l su

blux

atio

n0.

15 (

horiz

onta

l)B

est

vert

ical

cor

rect

ion

in 4

0% o

f pa

tient

s.

asym

met

ryC

aval

ier

0.90

(ve

rtic

al)

Inef

fect

ive

(und

erco

rrec

ted

in v

ertic

al p

lane

and

0.46

(ho

rizon

tal)

caus

ed l

ater

al d

ispl

acem

ent

of h

umer

al h

ead)

Bro

oke

1991

79A

P r

adio

grap

hH

arris

slin

g–0

.07

(ver

tical

)B

est

vert

ical

cor

rect

ion

and

mos

t co

nsis

tent

(n=

10)

Ver

tical

and

–0.1

6 (h

oriz

onta

l)ho

rizon

tal

Bob

ath

slin

g0.

47 (

vert

ical

)Le

ss e

ffec

tive

vert

ical

cor

rect

ion

and

dist

ract

ed t

hedi

spla

cem

ent

0.66

(ho

rizon

tal)

glen

ohum

eral

joi

nt i

n th

e ho

rizon

tal

plan

eA

rm t

roug

h/la

p-tr

ay–0

.78

(ver

tical

)Le

ss e

ffec

tive;

ten

ded

to o

verc

orre

ct.

Arm

cou

ld b

e0.

06 (

horiz

onta

l)po

sitio

ned

in l

ess

addu

ctio

n an

d la

tera

l ro

tatio

n




rotation100) 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 intointernal rotation, this must be reversed before thearm is abducted beyond 90°. Equally, in the sub-luxed shoulder, the humeral head should be relo-cated in the glenoid cavity before movement toavoid traction damage.59 A variety of physio-therapy techniques have been described61,62 manyof which are aimed at restoring normal alignmentand inhibiting muscle tone in the muscle groupswhich produce shoulder retraction but theirdetailed description is beyond the scope of thisreview. Some success has also been reported withantispasmodic drugs63 and with ice and heat.62,63,69

Electrical stimulationThe role of functional electrical stimulation

(FES) in management of both the upper andlower limb following stroke was reviewed byBinder-Macleod and Lee101 and its role in themanagement of HSP is currently the subject of aCochrane systematic review.102

In the meantime, we summarize �ve controlledtrials of FES in the management of the hemi-plegic shoulder (Table 6). FES aims to maintainmuscle bulk and tone in the �accid shoulder andpossibly enhance functional recovery throughcortical feedback. Some have used FES to pre-vent the development of subluxation in the �ac-cid shoulder,103,104 while others aim for reversal ofexisting subluxation.105–107 FES has been appliedeither to the posterior deltoid and supraspinatusmuscles,107 or to both,103,104,106 except inChantraine’s study105 which did not specify a site.Stimulation was continued for between four andsix weeks but the actual regimen and number ofhours per day varied markedly between studies.

Overall, FES produced encouraging effects onsubluxation, both for treatment and prophylaxis.Some also reported improvement in ‘motor func-tion’,104,105,107 although where speci�ed, this wasmainly power of abduction. The relationship withactual pain was not so clear, but three of the �vestudies reported some degree of improvement inHSP.104,105,107 Linn et al.103 expressed concern thatthe effects did not last after FES was discontin-ued. However, their study used the shortest reg-imen (four weeks). Chantraine’s larger study105

properties of the sling. Moreover, slings and sup-ports may reduce subluxation, but do they actu-ally reduce hemiplegic shoulder pain? The onlystudy to address this directly was a small prospec-tive study of strapping,97 which showed that theonset of HSP could be delayed in a populationof patients with new strokes.

To overcome the problem of compliance,Pinzur and Hopkins98 have promoted an opera-tion to reduce inferior subluxation by looping thelong tendon of biceps over the coracoid process.This was reported to provide complete pain reliefin 5/6 patients. However, this is clearly somethingto be considered only in chronic �accidity, andnot while there is any possibility that spasticitywill still develop.

In summary, given the evidence that severesubluxation may result in damage to soft tissuesand possibly even nerves, and given the intuitivenotion that a supported arm is less likely to beexposed to forces which produce subluxation,best practice would appear to advocate that thearm should be supported around the clock bywhichever method provides the best correction inthat individual. If nothing else, a sling or supportmay serve to alert staff to the need to handle thearm with care.

Passive range of movement and reduction ofspasticity

Early passive range exercise is generallyagreed to be an important measure to preventimmobility and soft tissue contracture.10 Again,the question is not whether it should be done, buthow? Improperly administered passive exercise,however, can cause impingement. The use ofoverhead exercise pulleys, in particular, has beencited as a cause of pain, impingement and evenrotator cuff rupture33 and has been positivelyassociated with the development of HSP99 – theyshould not, therefore, be used. Instead, passiverange exercises should be undertaken by atrained professional to ensure that the shoulderis moved with appropriate rotation of the scapulaand humerus to avoid impingement or damage tothe rotator cuff. It is important to remember,however, that ‘normal’ range becomes reduced inan older population.20 Maintenance of a freefunctional range of movement (100° �exion, 90°abduction, 30° lateral rotation, and 70° medial




Tab

le 6

The

use

of F

ES

in

the

man

agem

ent

of H

SP

and

sub

luxa

tion

Aut

hor

and

No.

of

subj

ects

Tim

e af

ter

Des

ign

Inte

ntio

nR

egim

enM

uscl

esS

igni

�can

t ef

fect

sye

arS

elec

tion

stro

ke o

nset

follo

w-u

p

Bak

er19

8610

6n

= 6

32–

36 w

eeks

RC

TTr

eatm

ent

ofIn

crea

sing

to

Pos

t. d

elto

idS

ublu

xatio

nS

ublu

xatio

nA

vera

ge 5

–731

tre

atm

ent

subl

uxat

ion

6 ho

urs/

day

for

AN

D(R

adio

grap

hic)

32 c

ontr

ols

6 w

eeks

supr

aspi

natu

sFU

: 3

mon

ths

Fagh

rin

= 2

6M

ean

17 d

ays

RC

TP

roph

ylax

isIn

crea

sing

to

Pos

t. d

elto

idS

ublu

xatio

n19

9410

4Fl

acci

d13

tre

atm

ent

6 ho

urs/

day

for

AN

D(R

adio

grap

hic)

shou

lder

13 c

ontr

ols

6 w

eeks

supr

aspi

natu

sP

ain

wea

knes

sFU

: 3

mon

ths

(Pai

nles

s R

OM

in

exte

rnal

rot

atio

n)M

otor

(Bob

ath

scal

es)

Linn

n=

40

With

in 2

day

sR

CT

Pro

phyl

axis

Incr

easi

ngP

ost.

del

toid

Sub

luxa

tion

1999

103

Flac

cid

20 t

reat

men

t2–

4 ho

urs/

day

AN

D(R

adio

grap

hic)

shou

lder

20 c

ontr

ols

for

4 w

eeks

supr

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peutic trial of NSAIDs, providing there are nocontraindications. Analgesic medication shouldbe withdrawn if not effective.

Local injection techniquesA recent survey from the Netherlands demon-

strated that most doctors believe that steroidinjections are effective in HSP.110 In reality, localinjection with corticosteroids is shown to give dis-appointing results in HSP, unless used speci�callyin the context of in�ammatory lesions such asrotator cuff or bicipital tendinitis, or tears withsecondary subacromial bursitis. Modest relief hasbeen obtained by injection of the subacromialbursa in some cases48 – presumably where rota-tor cuff impingement or in�ammation was one ofthe factors contributing to pain.

Dekker et al.113 obtained some reduction ofpain with intra-articular injection of triamci-nolone acetonamide in �ve of their seven patientsin an AB design study, but elsewhere the disap-pointing results from intra-articular steroid injec-tion have been attributed to pain resulting fromspasticity in the shoulder girdle muscles2 asopposed to in�ammatory causes within the jointcavity.

The popularity of local steroid injection prob-ably re�ects a misheld assumption that HSParises from the same in�ammatory pathology thatgives 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, wehave presented evidence for a range of other aeti-ological factors for HSP (malalignment, spastic-ity, etc.) which would not respond to the localanti-in�ammatory effects of corticosteroid injec-tion. In view of the likelihood that the atrophiceffects of repeated steroid injections will furtherweaken the cuff, we conclude that this form oftreatment should only be employed with extremejudiciousness. Symptomatic relief with an initialtest injection of lignocaine, or the use of T2-weighted MRI images14 may help to targetin�ammatory lesions and ensure that steroids areonly used where they are most likely to help.

The suprascapular nerve provides some of thesensory innervation of the shoulder. Suprascapu-lar nerve block has been used with some successin relieving resistant shoulder pain in rheumatoidarthritis,114 persistent rotator cuff lesions115 and in

had the longest follow-up period (two years) andhere the treatment effects were still evident forpain, 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 placebostimulation, but the effect on pain was not com-mented upon. Prada and Tallis109 have used acontingency electrical stimulator in the manage-ment of neglect. Whenever the patient moves thenonaffected arm, the device stimulates the fore-arm skin to draw attention to the affected arm.Preliminary results are promising, so if neglectdoes have any part to play in the causation ofHSP, 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 tooffer potential bene�ts, as an addendum to nor-mal therapy, for both the treatment, and proba-bly the prevention, of subluxation and itscomplications. The jury is still out, however, onother applications of electrical stimulation.

Oral analgesic medicationGiving symptomatic pain relief through the use

of simple analgesics or nonsteroidal anti-in�am-matory drugs (NSAIDs) is common practice inthe management of shoulder disorders both inthe general population22 and in patients withHSP.11,110 Ef�cacy of NSAIDs for short-termmanagement of shoulder pain in general has beensuggested by the results of a systematic review of19 trials.111 The authors found a superior bene�tover placebos in four trials, though differingselection criteria and a wide range of shoulderdisorders meant that evidence of bene�t in spe-ci�c 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 includingNSAIDs. They made more direct comparisonsbetween trials by calculating effect sizes for thesame reported outcome measures and concludedthat there is little evidence to either support orrefute the ef�cacy of common interventions forshoulder pain.

In the absence of clear evidence for the ef�-cacy of NSAIDs and simple analgesia in HSP, itseems reasonable to offer the individual a thera-




Conclusions and proposed ‘bestpractice’ for management of HSP

Despite the substantial attention paid to hemi-plegic shoulder pain in the literature it is stillpoorly understood and often inadequatelytreated. The purpose of this review was to clar-ify the mechanisms that produce hemiplegicshoulder pain and to examine the available evi-dence that informs best practice in the manage-ment of this dif�cult problem. So whatconclusions have we drawn?

Patients at high risk for developing HSPappear to be those with severe paralysis in theupper limb. Inappropriate handling techniquesmay increase the likelihood of traction injury,especially in the �accid shoulder, and wheredegenerative change in the rotator cuff predis-poses to trauma. Education of all staff and rela-tives involved in handling the patient is vital toprevent damage that may prolong hospital stayand increase disability. Careful hand-over tocommunity-based carers following dischargefrom hospital is also essential. Because of thediverse and multifactorial nature of HSP, suc-cessful treatment depends on careful evaluationand interpretation of the clinical signs with dueregard to the functional anatomy. While HSP

frozen shoulder.116 In the only study currently inthe literature to use this technique in HSP35 itfailed to provide complete pain relief. However,it was used as a diagnostic test, rather than atherapeutic manoeuvre, and in only three cases.Suprascapular nerve block is a simple, safe andinexpensive technique. In view of its potential,demonstrated in other contexts, to relieve painoriginating from the shoulder, a therapeutic rolein HSP is worthy of further exploration.

As described above, re�ex sympathetic dystro-phy (RSD) represents a speci�c subgroup ofHSP, requiring speci�c management in its ownright. Sympathetic blockade by stellate ganglionblock followed by intensive rehabilitation is citedas the most effective treatment by earlierauthors84,117 with surgical sympathectomy inrefractory cases.84 More recently, Braus et al.118

reported relief in 31/36 cases with low-dose oralcorticosteroids and this �nding was supported bya recent systematic review.119 Hamamci et al.120

reported a signi�cant reduction in pain andincreased range of movement in 25 patientstreated with salmon calcitonin, compared with 16control subjects. Once again formal controlledstudies are needed, but preliminary reports ofsuccess using noninvasive techniques merit fur-ther investigation.

The clear relationship between spasticity andshoulder pain, and the response of spastic shoul-der pain to surgical release2 (in resistant cases)and similarly to subscapular nerve block67 sug-gests that this is an area worthy of further explo-ration. Botulinum toxin has been used on othersites of the body to reduce localized spasticitywith good effect.121 To date there has been noformal trial of botulinum toxin injected into thesubscapularis, possibly because of the expense ofthe agent and the relative technical dif�culty ofsiting an injection. However, there is clearly aneed for further study in this area.

In summary, local steroid injections either tothe glenohumeral joint or the subacromial bursashould be avoided unless there is clear evidenceof an in�ammatory lesion. Nerve blocks mayhave a role to play in reduction of severe pain orsympatho-mimetic symptoms, and in spasticitymanagement the role for botulinum toxin needsfurther exploration. These and other less invasivetechniques require systematic evaluation.

Clinical messages

� Hemiplegic shoulder pain (HSP) is animportant condition, requiring co-ordinatedmultidisciplinary management to minimizeinterference with rehabilitation and opti-mize outcome.

� HSP broadly divides into ‘�accid’ and ‘spas-tic’ presentations – each requiring differentapproaches to handling, support and inter-vention. Management should vary accord-ingly.

� Education of all staff and relatives involvedin handling the patient is vital to preventdamage that may prolong hospital stay andincrease disability.

� Development of an ICP provides a method-ical approach to management and a soundbasis for prospective evaluation of interven-tions in the future.




traindications. Caution must be exercised forthose with a history of peptic ulceration, thosereceiving anticoagulation therapy or high-doseaspirin, and for elderly patients with borderlinerenal function. Timing of medication should beadjusted to the pattern of pain (e.g. night-timepain or pain on exercise) to obtain maximumbene�t.

Local injection with corticosteroid has limitedbene�t, except in the presence of active in�am-mation, and should be used judiciously asrepeated steroid injection produces tissue atro-phy which will further weaken the rotator cuffand 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 bene�t. Byblocking some of the sensory supply to the shoul-der, suprascapular nerve blockade may have arole as a pain-relieving procedure. Careful exam-ination may reveal evidence of autonomic dis-turbance such as colour, temperature or sweatingchanges that may suggest RSD, in which casesympathetic blockade or oral steroids may beconsidered.

As an important part of any integrated carepathway, careful assessment (if possible usingvalidated measures) should be repeated regularlyto monitor the treatment response. This is par-ticularly important in HSP where the nature ofthe condition is likely to change over time,requiring appropriate modi�cation of manage-ment strategies. To provide effective pain reliefit is helpful to know whether pain is constant, orworse at speci�c times such as at night, or duringphysiotherapy. Pain assessment is particularlydif�cult in the stroke population, so a battery ofsimple tools accessible to people with communi-cation, perceptual and cognitive dif�culties isrequired to follow progress.

AcknowledgementsThe authors would like to thank the John

Squire Library staff at Northwick Park Hospitaland Tabi Turner-Stokes for help with gatheringthe literature. Also staff and colleagues on theRegional Rehabilitation Unit for support andhelpful discussion. The preparation of this articlewas supported �nancially by an audit grant fromthe 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 tomanagement. At one end is the �oppy subluxed(‘�accid’) shoulder, requiring careful support toavoid damage to soft tissues and nerves. At theother end of the spectrum is the stiff (‘spastic’)shoulder associated with soft tissue contractureswhich hold the arm in a position of adduction andinternal rotation. Over time, patients mayprogress from the �rst towards the second. Fail-ure to recognize these differences and theirrespective requirements for management mayexplain some controversies in the literature.

The ‘�accid’ shoulder requires particular carein handling, even in the absence of pain. The armshould be appropriately supported at all times,with a wheelchair arm support by day and pillowsat night. In the preferred position the shoulder isprotracted with the arm forward, in slight abduc-tion and neutral rotation. The wrist should be inneutral or slight supination, and the �ngersextended, but a range of different approved posi-tions may be determined for each patient. Anindividually selected shoulder brace or sling mayoffer support as the patient gets onto their feet,as well as reminding staff of the need for care inhandling. Neurophysiotherapy techniques may beemployed to restore alignment and maintainfunctional range of movement, but with care toavoid 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 moreacutely painful and may respond to analgesic orantispasmodic medication. Positioning is impor-tant here to try to relieve spasticity. Externalrotation and abduction of the arm are to beencouraged once spasticity in the medial rotatorsof the shoulder has been reduced by properlytrained staff. Overhead exercise pulleys are to beavoided at all costs. In resistant cases, soft tissuerelease may be considered, but spasticity is oftenself-limiting with appropriate treatment, and fur-ther work is required to explore the role of lessinvasive procedures such as nerve blockade orbotulinum toxin to provide localized relief ofspasticity.

A therapeutic trial of NSAIDs or simple anal-gesia may be offered, providing there are no con-




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