d i s a b i l i t y a n d r e h a b i l i t a t i o n , 2001 ; v o l . 23, n o .

13, 549 558

REVIEW

Contractures in orthopaedic and neurological

conditions : a review of causes and treatment
S. E. FARMER * and M. JAMES

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Orthotic Research and Locomotor Assessment Unit, Robert Jones and Agnes Hunt Orthopaedic and
District NHS Hospital Trust, Oswestry, Shropshire SY10 7AG, UK
Centre for Health Planning and Management, University of Keele, Keele, Staordshire ST5 5BG, UK

Accepted for publication : December 2000

Abstract
Purpose : To examine the techniques used for the treatment of
contracture in the context of current scienti c knowledge of
muscle.
Method : Synthesis of data available from MEDLINE,
RECAL, EMBASE, the Cochrane Library and relevant texts.
Results : The development of contractures through immobilisation, muscle weakness and spasticity is described. The eects
of passive stretching, continuous passive movement, serial
plastering, splinting, electrical stimulation, botulinum injections and surgical tenotomies in the treatment of contractures in persons with neurological and orthopaedic conditions are identi ed. The strengths and weaknesses of these
modalities are discussed.
Conclusion : Predisposing factors persist after treatment of
contractures thus for treatment to be eective long-term
management programmes need to be developed. New treatment
techniques, used in series or combined, oer the prospect of
improved management of contracture. Scienti c and clinical
research is needed to investigate the eect of contracture
treatment.

Information on contractures has been obtained

from literature between 1966 2000 using MEDLINE,
RECAL, EMBASE and the Cochrane Library databases
for keywords : contractures, cerebral palsy, traumatic
brain injury, passive movement, serial plastering,
orthoses, electrical stimulation, and muscle lengthening.
In this paper a summary description of normal muscle
structure and growth will precede a section which draws
together factors which predispose to the development of
contractures. In the following section treatment
modalities are described and critically appraised. The
format of reporting on each technique and outcome with
authors comments has been used instead of results and
discussion sections to facilitate linking experimental
physiology to each speci c treatment modality ; thus
deriving the strengths and weaknesses of these
modalities. The conclusion then attempts to highlight the
most eective means of treating contractures whilst
suggesting the potential for further development of
treatment techniques.

Introduction
The purpose of this paper is to review literature with
regard to muscle physiology and the causes of contracture. Contractures by their nature limit the mobility
of joints and therefore impact on the lifestyle of
individuals with contractures. The health economic issues
in providing treatment for contractures impinge evermore on those providing care in a rehabilitation context.
A number of treatment modalities are used to reduce
contractures. These treatments will be considered in the
context of the physiology and pathology described,
discussing how treatment can be optimised.
* Author for correspondence ; e-mail sybil.farmer!
tr.wmids.nhs.uk

rjahoh-

Muscle: structure and growth

A number of structures are implicated when a joint is
described as having a contracture: these include the joint
capsule, joint ligaments, the muscles and their tendons
which adapt to the deformed position.
Muscles are complex structures which consist of the
contractile tissue" , # and connective tissue$ . The working
mechanism of contractile tissue consists of myosin and
actin myo laments which interdigitate; sliding together
as the muscle contracts and apart as the muscle lengthens.
Units of this contractile tissue, the sarcomere, in series
form myo brils. Bundles of myo brils form muscle
bres. The bres are aggregated together to form fascicles
and nally the entire muscle. Connective tissue, the

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S. E. Farmer and M. James

perimysium, the endomysium and epimysium contain
these brils, bres and muscle tissues.
Connective tissue is comprised of collagen and elastic
bres. Collagen has great tensile strength and is relatively
inextensible. Collagenous bres are arranged in bundles
and at rest are wavy. The collagen molecule consists of
three polypetide chains which forms a triple helix : these
molecules are overlapped to form the micro brillar
tubule around which is wound the surface band. This
description by Inoue & Leblond% is taken from work on
connective tissue of mice and has yet to be con rmed in
humans. $ Elastic bres are mechanically elastic and
occur in association with collagen bres.
A muscle can therefore be modelled as a contractile
component with elastic elements in series and in parallel
with the contractile tissue.&
During normal development muscles grow maintaining a length which is optimal for length} tension
characteristics and thereby reduces the likelihood of
overstretching and damage. This is achieved by sarcomeres being added to the ends of myo brils. Rate of
bone growth, the amount of stretch, the presence of
hormones (growth hormone, insulin and testosterone)
and nutritional status in uence normal muscle growth.
With maturation muscles hypertrophy ; the myo brils
split lengthwise and there is a resultant increase in crosssectional area.
If muscle growth or replacement is inadequate then a
contracture will develop ; in describing the factors
in uencing protein synthesis an overview of factors
which limit normal growth follows.
Muscle protein is continuously recycled. The half life
of contractile proteins is 7 15 days : so muscles can easily
adapt to new demands or lack of demand.( The number
of muscle bres does not change under normal conditions
but cross-sectional area increases as the number of
myo brils within muscle increases. In pubescent boys
under the in uence of testosterone cross sectional area
and muscle strength increase. Exercise also stimulates
muscle hypertrophy with eccentric exercise providing the
strongest stimulus.) Proteins can be accumulated during
growth or exercise by an increased rate of synthesis
and} or a reduction in their break down rate.
Disuse of skeletal muscle leads to atrophy. Atrophy
can be due to reduction in the number of sarcomeres
lengthwise or to a reduction in the cross-section area of
the muscle bres. Goldspink* showed in a study using
young rats that when soleus and extensor digitorum
longus (EDL) were immobilised in a shortened position
the muscles underwent atrophy showing net loss of
muscle protein. There was a higher rate of protein
turnover in soleus than in EDL. This was thought to be
550

due to the higher level of activity in soleus shown in emg

studies which contrasts with the lower level of activity
related recruitment of EDL." !
The development of contractures
In this section the factors which produce joint
contractures are described and discussed with particular
reference to the eects of immobilisation, muscle
weakness or paralysis and spasticity.
Muscle and connective tissue are both aected in the
presence of contracture. Sarcomeres are lost from the
ends of myo brils and connective tissue can adaptively
shorten and lose elasticity. In the literature contractures
are normally described in the context of a speci c
pathology ; this paper uses as its focus the physiology of
the development of contractures across neurological and
orthopaedic conditions in which there is a high incidence
of contracture. This is demonstrated in cerebral palsy by
numerous papers evaluating surgical treatment of contracture in children with cerebral palsy." " , " # , " $ , " % Joint
contracture occurs following craniocerebral trauma, with
Yarkony et al." & reporting that in 75 consecutive referrals
84 % had contractures. In haemophilia," and after
stroke" ( over 50 % of patients studied had contractures.
In orthopaedics contractures occur after fracture treatment immobilisation, in hemimelia, and in other congenital deformities including arthrogryposis ." ) It is
acknowledged that contractures also occur in rheumatoid arthritis, following burns and as a complication
of limb amputation and in many other conditions when
additional factors including joint degeneration, scar
tissue and muscle imbalance further complicate management.
In neuromuscular conditions immobilisation, muscle
weakness or paralysis and spasticity are the three main
factors leading to the development of contractures
variously aecting the joint itself, contractile tissue
and} or connective tissue.
With immobilisation
c h a n g e s w it h in t h e jo in t
Immobilisation of a joint may be necessary to allow
healing after a fracture and may occur with disorders
causing joint pain including degenerative and in ammatory conditions.
With prolonged immobilisation of a joint, bro-fatty
connective tissue proliferates and encroaches into the
joint space. These changes are rst seen at two weeks. As
immobilisation continues brous adhesions occur and
further aect the mobility of the joint. Prolonged

Orthopaedic and neurological conditions

immobilisation also aects the joint cartilage ; where two
surfaces are in contact there is thinning at the point of
contact. " *

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e f f e c t s o n m u sc l e a n d t e n d o n l e n g t h
Regulation of sarcomere number is considered to be
an adaptation to changes in functional length of the
muscle.( Muscles immobilised in a lengthened position
gain sarcomeres whereas the muscle immobilised in the
shortened position lose sarcomeres.# ! There do however
appear to be age related eects. In rabbits who are not
fully grown and very young rabbits after an initial period
(5 days) when sarcomere numbers increase this reduces
and any further increase is due to increased tendon
length.
e f f e c t s o n c o n n e c t iv e t is s u e
If joints are immobilised for any length of time then
connective tissue loses its extensibility# " . The immobility
allows development of abnormal cross linking between
connective bres.$
After a muscle is immobilised in a shortened position
there is increased resistance to passive stretch. This is
probably due to connective tissue accumulation. During
immobilisation connective tissue is lost at a slower rate
than contractile tissue: therefore there is a relative
increase in the proportion of connective tissue in a
muscle after a period of immobilisation.(
When immobilisation is used in conjunction with
electrical stimulation then there is no connective tissue
accumulation. This implies that contractile activity is a
key factor in maintenance of normal proportion of
connective tissue within the muscle.# #

An imbalance occurs between the strengths of agonists

and antagonists. As the child becomes weaker more time
is spent in sitting than standing and such positioning
predisposes to hip and knee exion contractures and
equinovarus deformity of the feet. These deformities are
common in DMD.
in p a r a l y s is
A muscle is paralysed when it lacks normal innervation : tone is absent and the muscle tissue atrophies
through disuse. Eects of denervation include reduction
in size of bres, necrosis of some bres and slowing of
contractions produced by direct stimulation of the
muscle.# %
Goldspink et al.# & show that if the soleus muscle of a
cat is denervated and held in a lengthened position there
are 25 % more sarcomeres in series, whilst if immobilised
in a shortened position then 35 % of sarcomeres in series
are lost. Four weeks post removal of the plaster these
denervated muscles have returned to normal length.
In spasticity
l o ss o f sa r c o m e r e s
In cerebral palsy, after traumatic brain injury and in
stroke, spasticity produces imbalance when spastic
muscle continuously contracts pulling the aected limb
into a deformed posture which becomes a contracture.
Tetanic contraction can be used to simulate spasticity.
Huet de la Tour et al.# injected toxin into the soleus of
one limb of guinea pigs, producing a tetanic contraction
in this limb. This produced a marked loss of sarcomeres
in this muscle which was greater than that from
immobilisation alone.

With muscle weakness

in c r e a s e d m u s c l e s t if f n e s s

An imbalance between the agonists and antagonists

can occur when a muscle is paralysed or considerably
weakened as in spina bi da, spinal cord injury or
poliomyelitis. When a muscle is unopposed by an
antagonist then that muscle becomes shortened and joint
contractures develop.
Contractures occur in progressive neuromuscular
disease : the changes in Duchenne Muscular Dystrophy
(DMD) are characterised by replacement of muscle
bres with collagen and fatty tissue. The remaining
muscle bres are chronically shortened. Collagen within
the endomysium, perimysium and epimysium proliferates and restricts joint motion.# $

In addition to the shortening of the myo bril by loss

of sarcomeres from the ends it has been suggested by
Carey and Burghardt# ( that there may be some alteration
in the resting length of the sarcomeres themselves. In
normal muscle at rest the myosin and actin within a
sarcomere have some degree of overlap. These thick and
thin laments are able to slide over each other. This is
achieved by the cross bridges of the myosin attaching to
the actin brie y to propel the myosin along the actin in
the presence of Adenosine Triphosphate (ATP). When
the movement is towards the centre of the sarcomere
then a concentric contraction occurs. In spasticity it is
suggested that the mechanism for attaching and
551

S. E. Farmer and M. James

detaching is disordered. The inherent increased stiness
in spastic muscle is due to an increased amount of
interdigitation between actin and myosin. Dynamic
eects are likely to be due to premature attachments
between myosin and actin or their failure to disengage
completely after activity. This status of increased overlap
between the laments would presumably reduce the
range through which the muscle can contract concentrically.

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c h a n g e s in c o n n e c t iv e t is s u e
The relative immobility of the limbs in cerebral palsy
and other neurological conditions predispose to loss of
elasticity and relative increase in the connective tissue
within the muscle. Tardieu et al.# ) plotted ankle angle
against torque to demonstrate the hypoextensibility in
the calf muscles of children with cerebral palsy.
Treatment techniques
A number of conservative and surgical techniques are
used to treat contractures. Much of the literature on this
subject devotes itself to reporting ndings of a treatment
for a speci c joint in a speci c condition.
In considering the eects of treatment modalities the
following general principles should be considered. Sarcomeres are gained when muscle is held in a lengthened
position and these gains are increased with stretching or
electrical stimulation. If, however the muscle is held in a
shortened position then sarcomeres are lost, electrical
stimulation or tetanic muscle contraction increases this
loss.
Connective tissue accumulates with immobility but
this eect is ameliorated by contractile activity. Connective tissue when immobile forms crossbridges between
collagen bres and thus its elasticity is reduced.
Muscles produce force and movement and these
properties can be adversely aected by contracture and
contracture treatment.
Treatment should therefore be directed to maintain or
increase contractile and connective tissue length whilst
reducing stiness and loss of elasticity. Muscle properties
of force generation need to be `normalised through
treatment.
Connective tissue has time dependent mechanical
properties. # * Stress relaxation occurs when tissue is held
under tension at a constant length : with time there is loss
of tension. If a constant force is applied then lengthening
occurs ; this eect is called creep.
Connective tissue is aected by the way it is stretched.
High force short duration stretch at normal temperature
552

produces elastic response (i.e. recovery of normal length).

A prolonged low force stretch at a high temperature
produces plastic deformation. If the tissue is allowed to
cool before the tension is released then the lengthening is
maintained. $ ! The connective tissue is maximally weakened by high force; low temperature stretches whereas
low force applied at higher temperature produces
minimal structural weakening.$ "
The following sections reviews each technique used
and then comments on the basis of the underlying
physiological processes.

Passive stretching
Passive stretching is a technique frequently used by
physiotherapists . To stretch a joint, the joint is positioned
at the limit of range of movement and overpressure
sustained. Ada et al.$ # state that although therapists have
been providing passive stretching to patients with
contractures there is no scienti c basis for the frequency
and duration of this treatment.

c o m m e n t
The eectiveness of passive stretching will depend on
the nature of the contracture and its predisposing factors.
Williams$ $ has shown that daily stretching of 30
minutes in an otherwise immobilised limb prevents
sarcomere loss. Tardieu et al.$ % monitored the amount of
time that a spastic muscle was in a stretched position
during activities of daily living. This position was
determined by measuring (in the laboratory) the minimum angle of dorsi exion at the ankle at which a
dorsi exing torque could be measured in an electrically
silent muscle. They found that contractures did not occur
when muscles were in a lengthened position for more
than six hours per day. Thus it is di cult to counteract
the dynamic eects of spasticity by passive stretching.
Passive stretching does provide a low force stretch so
it could aect connective tissue but work by Warren$ "
showed changes after 50 minutes sustained stretching.
This length of time exceeds that normally used for
passive stretching to a single structure. Thus it would
seem that for passive stretching to be eective it must be
maintained for su cient time to overcome factors which
predispose to contracture.
Clinicians would perhaps be wise to consider other
modalities, which prolong the stretching time especially
when certain static postures predominate or when
movement patterns fail to utilise a normal range of
movement.

Orthopaedic and neurological conditions

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Continuous passive movement (CPM)

CPM is used in the post-operative management of
total knee replacements. Worland et al.$ & report no
dierence in clinical outcome for CPM users and those
receiving professional therapy but reduced costs for use
of CPM. Ververeli et al.$ report that no CPM users
required knee manipulation for limited knee exion in
contrast to ve non-CPM users. Pope et al.$ ( sounds a
note of caution as they nd that their CPM patients have
increased blood loss and require more analgesia.
CPM has been used to maintain range following
surgery to resect pathological ossi cation of knee and
elbow in patients with post traumatic brain injury.$ ) , $ *

c o m m e n t
CPM seems to oer the prospect of reduced joint
in ltration whilst limiting the opportunity of abnormal
crossbridging within the collagen. The velocity of
stretching is a factor in spasticity ; thus the application of
CPM in neurological conditions would be dependent on
setting the speed of passive motion at a level below the
level which induces a spastic response.

Serial plastering
In this technique the joint is held at the limit of the
range of movement in Plaster of Paris or other `plastering
material . The plaster is changed at regular intervals with
the joint being held at the new limit of range. Techniques
for using serial casting in the management of spasticity in
the head-injured adult were described by Booth et al.% !
`Drop out casts are used to allow movement into the
desired range of movement but to limit the progression
of deformity. Their study reports increased range of
ankle dorsi exion and decrease in plantar exor tone
following the use of short leg casts for patients with
cortical lesions. Hoer et al.% " discussed the management
of contractures in cerebral palsy recommending serial
plastering when muscles fail to respond to passive
stretching. Cusick% # describes the application of serial
casts to the lower limbs. A single case study was used to
demonstrate the improvement in knee contractures in a
child with spastic diplegia treated with serial long leg
plasters for 45 days. The exion contractures prior to
casting were 40 bilaterally and after treatment full
extension of the right leg was found. A residual 5
contracture remained in the left knee. Brouwer et al.% $
indicate that after 3 weeks serial casting that there was an
increase in range of dorsi exion without associated loss

of plantar exor strength. A further positive outcome was

a shift in the length tension curve into dorsi exion.
Cottalorda et al.% % also show similar results of increased
dorsi exion, but report re-occurrence of equinus deformity in half the limbs studied at 18 months.

c o m m e n t
Serial plastering, night splint and xed splints hold
joints in a xed position. On application there is some
stretching but this is not maintained as connective tissue
`creeps away from the deforming force ; thus after a
short while no stretch is being applied to immobilised
tissues. In serial plastering there is continuous immobilisation which will allow the stretched muscles antagonist to atrophy and shorten. `Drop out plasters can
be used to overcome this problem when complete
immobilisation is unnecessary. The eects on the
antagonist as well as the agonist need to be considered in
any such treatment regime.
Tardieu and Tardieu% & indicate that in young animals
immobilisation in plaster produces an increase in tendon
length with a decrease in muscle belly length. In current
clinical practise there is a tendency to use serial plastering
in younger children Cottalorda et al.% % ; it may be that the
increase in dorsi exion reported is due to an oset of the
range into dorsi exion due to tendinous lengthening
similar to that seen in young rabbits.# ! Equinus recurs as
the spasticity persists reducing the numbers of sarcomeres in series and adapting to the new tendon length.
The new situation gives a further reduction in the total
range of ankle motion.
Clinicians should be aware that immobilisation for
prolonged periods although producing apparent bene ts
may in the long term produce alteration in muscle}
tendon ratio and consequent shift in angle of peak
torque. This is in addition to the muscle atrophy and
consequent muscle weakness together with the loss of
elasticity due to connective tissue accumulation.

Splinting
Orthoses can be used to hold a joint at the limit of
range. Some commercially available splints (e.g. knee
immobilisers) are readily available.% Bespoke night
splints are made from a cast of the aected joint which
is positioned at the limit of the range of movement. These
splints are used to hold the joint as near as possible to the
limit of range of movement. Di culty with application
usually prevents the joint being positioned at the limit of
range. When range is gained then a more corrective
553

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S. E. Farmer and M. James

splint has to be made. Anderson et al.% ( described a
technique using high density foam to treat knee contractures. Improvements in knee contractures were
achieved by using these splints at night.
Bonutti et al.% ) describe a technique which applied a
static progressive stretch to the elbow. The orthosis used
permitted an incremental displacement to be applied to
the joint at successive applications. Gelinas et al.% * used
a turnbuckle splint on elbow contractures, acting into
exion or into extension. Their subjects had post trauma
elbow contractures with 11 of 22 subjects studied gaining
a functional range of elbow movement (30 130 and a
further eight subjects showed some improvement. There
were however di culties with compliance with the regime
of wearing the splint 20 hours per day to extend the
principally limited range of motion.
More recently the Dynasplint has been developed and
used in the treatment of contractures.& ! The system when
applied to the knee can be set to resist exion with a coil
spring but the authors report a varied response to the
application of the splints for 3 hours on 5 days per week
for a period of 5 months. They were not able to
demonstrate clear bene t from the use of these splints
with the regime followed in their study.
In a case study, Moore et al.& " use a dynamic splinting
system to treat contracture in a child with arthrogryposis .
Subsequently researchers& # ,& $ have used this technique of
a bespoke orthosis (the contracture correction device,
CCD) which incorporates a gas spring to provide a
continuous stretch. Gas springs provide a force which
changes little through its range of action which the
authors indicate allows a relatively constant force to be
applied to the contracted joint via this orthosis. Early
results reported indicate that some correction of contracture can be achieved by using the orthosis for an
hour per day over a 3 months time period.& %
c o m m e n t
Splints can be used for longer periods of treatment
than is available for passive stretching. They are removed
to permit stretching of the antagonists, thus maintaining
sarcomeres, and allow some normal activity to reduce
connective tissue accumulation thus reducing the risks
associated with immobilisation.
Dynamic splints (e.g. the turnbuckle splint) have an
advantage over serial plastering in that they can
immobilise the limb at the limit of range.
The contracture correction device provides a continuous stretching torque ; takes up the connective tissue
creep and thus is eective throughout the period of
application.
554

Since the CCD is a custom made orthosis, correct

alignment for stretching para-joint structures is achieved.
The torque can be set at a level appropriate to the
condition and size of subject which can be overcome by
voluntary muscle contraction thus permitting intermittent stretch of the antagonists.& %
Further basic research is required to clarify the eect
of continuous stretch on muscle and connective tissue.
Electrical stimulation
e l e c t r ic a l s t im u l a t io n a n d m u s c l e l e n g t h
Electrical stimulation has been used for assessment of
the eect of contractile activity on sarcomere numbers.
When a muscle is stimulated in a shortened position then
sarcomeres in series are lost. When muscle in an
unrestrained limb is stimulated there is still some loss of
sarcomeres. This is thought to be due to the eect of the
contraction tending to hold the muscle in a more
shortened position than normal.# # Passive stretching plus
electrical stimulation, however, produced a 40 % increase
in muscle weight after 5 days `treatment in rabbits.& &
Thus stimulation and passive stretching has a greater
eect than stretching alone.
e l e c t r ic a l s t im u l a t io n in t h e t r e a t m e n t o f
c o n t r a c t u r e s
Pandyan and Granat& used electrical stimulation to
treat exion contractures in the hemiplegic wrist. After
two weeks electrical stimulation their 11 hemiplegic
subjects treated showed improvements in passive range
of wrist extension. These bene ts were much reduced two
weeks after the treatment was discontinued.
Overnight low-intensity electrical stimulation was
applied to the leg muscles of six children with mild
cerebral palsy. There was a signi cant improvement
noted in these childrens Peabody Developmental Motor
Scales scores. In their discussion the authors allude to
muscle growth but did not report any changes in muscle
length following the treatment. They also noted that
when electrical stimulation was withdrawn for 6 months
there was uniform loss in scores.& (
e l e c t r ic a l s t im u l a t io n t o p r e v e n t m u s c l e a t r o p h y
Low frequency electrical stimulation has been shown
by Gibson et al.& ) to prevent quadriceps atrophy. When
immobilised in long leg plasters for tibial fractures, the
cross-sectional area of quadriceps muscles in men who
used electrical stimulation was comparable to controls

Orthopaedic and neurological conditions

but reduced in men, who did not use electrical stimulation, after similar injuries.

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c o m m e n t
Work with animal models described by Goldspink and
Goldspink & & indicate the potential for developing electrical stimulation techniques for the treatment of contractures due to loss of muscle protein. Gibson& ) has
shown that electrical stimulation can be used to overcome
the tendency for muscles to atrophy when immobilised.
Thus where immobilisation is necessary electrical stimulation could be used to reduce unwanted eects.
Electrical stimulation does appear to oer the prospect
of reduction in contracture whilst treatment is
continued. & A predisposing factor in this condition is
that the wrist joint is aected by gravity and taken into
exion. It may therefore be of bene t to use a
complementary splinting regime.
Botulinum toxin
Botulinum toxin is used to temporarily paralyse spastic
muscles. It is used to treat the spasticity which if not
relieved leads to the development of contracture.
Cosgrove and Graham & * showed that in the hereditary
spastic mouse the development of a contracture of
gastronemius did not occur in the muscle injected with
Botulinum toxin A. In the spastic mice not injected with
Botulinum toxin there was a reduction in muscle length
and an increase in tendon length compared to normal
mice. Spastic injected mice showed no signi cant
dierence in tendon or muscle length compared to
normal mice.
In subsequent work Cosgrove et al. ! described the use
of botulinum toxin in the management of the lower limb
in children with cerebral palsy indicating changes in
dynamic ankle motion towards normal values at 4 weeks
post paralysing injection. There is some regression to
pre-injection values at 16 weeks. Thompson et al. " used
musculoskeletal modelling to measure increases in length
in short hamstrings after injection with Botulinum toxin.
c o m m e n t
Botulinum toxin in temporarily relieving spasticity
does permit exstrinsic stretching of the dynamically
contracted muscle. This stretching can be due to the
eects of its antagonist activity, through the eect of the
ground reaction force (producing in the case of the
spastic mouse a dorsi exing moment about the ankle) or
by the use of other complementary modalities. (e.g. POP

casts # ) As the spasticity returns after the eect of the

injection wears o then there is a tendency for the
contracture to return. Repeated injections have been
used to sustain improvement $ .
A key advantage of this technique may be that the
normal ratio of muscle to tendon is maintained thereby
having the potential to maintain the same peak force
point in the range of movement.
Surgery
Numerous surgical procedures to lengthen shortened
muscles in cerebral palsy are described in the literature.
Bleck % describes many surgical techniques. The work of
Damron et al." # and Salsa et al." $ report on Tendoachilles
lengthening ; Dhawlikar et al. & and Damron et al.
report on hamstring lengthening : both muscles show a
reoccurrence of contracture after surgery. For some
children the eect of TA lengthening is a calcaneus
deformity due to overlengthening. ( Truscelli et al. ) link
the eectiveness of tendoachilles lengthening with the
mechanism producing the contracture. Outcome can be
unpredictable when dorsi exor and plantar exor spasm
is unequal.
Abel et al. * report on 30 children with spastic diplegia
who had muscle tendon surgery, nding that the primary
kinematic change is a shift in sagittal joint position with
minimal eects on overall excursion.
Muscles, which are shown to be acting inappropriately,
are surgically transferred. Rectus Femoris is transferred
to semimembranosus" " and Tibialis Posterior subjected
to a split tendon transfer around the hindfoot.( !
Baker( " looked at the eects of tenotomy on rat soleus
muscle. The muscle bellies were shortened, initially due
to shortening of the sarcomeres but by 4 weeks the
number of sarcomeres in series was reduced causing the
experimental muscles to show a 50 % reduction in muscle
belly length. Tardieu et al.( # in their work on cats
tendoachilles nd that at 7 months post elongation there
was a decrease in the muscular part and increase in the
tendinous part. Thus the action of muscle is aected by
surgery. Delp and Zajac( $ used a computer model to
study how the force generating capacity of muscles is
aected by surgical tendon lengthening. They show that
by lengthening lower limb muscles by 2cm or less that the
muscle force is reduced by 50 % . Hip muscles are less
sensitive to length change.
Damiano et al.( % studied the eect of hamstring
lengthening on quadriceps and hamstring strength,
nding that hamstring strength declined after surgery
but increased with time returning to preoperative values
by 9 months.
555

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c o m m e n t
Surgical lengthening gives relief to muscle shortening
in the short term and provides a therapeutic opportunity
for re-education of movement. In addition to the
lengthening eect per se there is also the reduced
sensitivity to stretch which this additional length
produces. Gage( & and Sutherland ( recommended multilevel surgery to release soft tissues at hips, knees and
ankles simultaneously together with the correction of
bony deformity.
Leiber( indicates that isometric force varies as a
function of muscle length. He refers to earlier work by
Gordon et al.( ( who described the length tension curve of
a single sarcomere. The force generated is maximal when
the sarcomere is at the mid-point between its maximum
and minimum length. Surgery to the tendon will tend to
move this point with consequent oset in the angle at
which peak force can be generated. Problems encountered with surgical lengthening include the reduction
of muscle power and an altered range of motion. Muscle
strength can be regained with muscle strengthening
exercise. The alteration in peak force angle may limit the
eectiveness of such treatment.
There is a tendency for shortening to re-occur which
requires further management. Although passive
stretching and static splints are the most commonly used
modalities at present they do not appear to be the most
eect in addressing contracture. Alternative complementary techniques (e.g. dynamic splinting) may be more
eective in maintaining improvement in range of movement.
Patrick ( ) describes intramuscular psoas tentomy and
Saraph ( * reports on the Baumann procedure which
lengthens the intermuscular gastronemius fascia. Such
techniques may address the accumulation of connective
tissue and appear to do so without aecting the power
generating capacity of these muscles.
Conclusion
Joint contractures are a common problem which
impedes the rehabilitation of patients following traumatic brain injury, stroke and fractures. Children with
cerebral palsy, spina bi da and arthrogyrposis have
progressive contractures that inhibit function and limit
their development. Treatment modalities include passive
stretching, serial plastering, splinting, botulinum toxin
injections, electrical stimulation and surgery. Each
modality has its positive and negative eects and must be
considered in the case speci c context.
Contractures can be prevented by the maintenance or
increase in numbers of sarcomeres in series, together with
556

the maintenance of tendon length and connective tissue

elasticity. Sarcomere numbers are maintained by
stretching and by electrical stimulation when the muscle
is held in a lengthened position. Immobilisation in a
lengthened position for a muscle maintains that muscle
length but may cause loss of sarcomeres from its
antagonist and risks connective tissue accumulation and
loss of elasticity. Connective tissue does not appear to
accumulate in the presence of contractile activity. Plastic
deformation of connective tissue is achieved by prolonged low force stretching, and enhanced when connective tissue is warmed prior to stretching and cooled
prior to release of stretch.
Contractures require long-term management when
certain conditions occur which cause progression of or
re-occurence of contractures. Passive stretching and
static splinting have limited eectiveness whereas dynamic splinting (CCD) oers the prospect of continuous
stretching during its application. Self-administered
orthoses oer the user autonomy. The prospect of
limiting the time for interventional treatment of the
contracture to part of the day is likely to improve
compliance. Immobilisation and surgery are potentially
damaging to muscle and connective tissue. Some surgical
techniques lengthen tendon but spasticity tends to
shorten the contractile tissue. Techniques which reduce
muscle stiness but retain muscle function prove more
successful in the treatment of contracture.
New ways of managing contractures can be developed
from recent advances in splinting, electrical stimulation
techniques and the use of botulinum injections. By
providing eective mechanical stretching (using CCDs),
complementing this with reduction of spasticity (with
botulinum toxin injections) and using electrical stimulation to further increase muscle length ; these techniques
may allow resolution of contractures. Multi-modality
treatment regimes need to be developed and tested. The
reasons for adopting new treatment modalities need to
be understood and evaluated by further clinical research.
References
1 McComas AJ. The muscle bre. In : Skeletal Muscle : Form and
Function. Champaign IL : Human Kinetics 1996 ; 3 18.
2 Alter MJ. Contractile components of muscle ; limiting factors of
exibility. In : Science of Flexibility Second Edition Leeds : Human
Kinetics 1996 ; 17 34.
3 Alter MJ. Connective Tissue ; A Limiting factor of Flexibility. In :
Science of Flexibility Second Edition Leeds: Human Kinetics 1996 ;
39 57.
4 Inoue S, Leblond CP. The micro brils of connective tissue : I.
Ultrasructure. American Journa l of Anatomy 1986 ; 176 : 121 138.
5 Rothwell J. Mechanical properties of muscle. In : Control of human
voluntary movement London : Chapman and Hall 1994 ; 10 17.
6 McComas AJ. Muscle Formation. In Skeletal Muscle : Form and
Function. Champaign IL : Human Kinetics 1996 ; 68 72.

Disabil Rehabil Downloaded from informahealthcare.com by University of Sussex Library on 10/12/12

For personal use only.

Orthopaedic and neurological conditions

7 Goldspink G, Williams P. Muscle Fibre and Connective Tissue
Changes Associated with Use and Disuse. In : Ada L & Canning C
(eds) Key Issues in Neurological Physiotherapy. Oxford :
Butterworth Heinmann 1990 ; 197 218.
8 MacDougall JD. Morphological changes in human skeletal muscle
following strength training and immobilization. In NL Jones, N
McCartney, AJ McComas (Eds) Human Muscle Power Champaign,
IL : Human Kinetics, 1987 ; 369 288.
9 Goldspink DF. The In uence if Immobilization and Stretch on
Protein Turnover of Rat Skeletal Muscle. Journal of Physiology
1977 ; 264 : 267 282.
10 Goldspink DF. The in uence of contractile activity and nerve
supply on muscle size and protein turnover. In : D Pette (Eds)
Plasticity of Muscle. New York : Walter de Gruyter 1980 ; 525 539.
11 Ounpuu S, Muik E, Davis RB, Gage JR, DeLuca PA. Rectus
Femoris Surgery in Children with Cerebral Palsy. Part 1 : The Eect
of Rectus Femoris Transfer Location on Knee Motion. Journal of
Pediatric Orthopaedics, 1993 ; 13 : 325 330.
12 Damron TA, Greenwalk TA, Breed AL. Chronologic Outcome of
Surgical Tendoachilles Lengthening and Natural History of
Gastroc-Soleus Contracture in Cerebral Palsy. Clinical Orthopaedics and Related Research 1994 ; 301 : 249 255.
13 Sala DA, Grant AD, Kummer FJ. Equinus deformity in cerebral
palsy : recurrence after tendo Achillis lengthening. Developmental
Medicine and Child Neurology 1997 ; 39 : 45 48.
14 Rethlefsen S, Tolo VT, Reynolds RA, Kay R. Outcome of
hamstring lengthening and distal rectus femoris transfer surgery.
Journa l of Pediatric Orthopaedics B 1999 ; 8 : 75 79.
15 Yarkony GM, Sahgal V. Contractures: A major complication of
craniocerebral trauma. Clinical Orthopaedics and Related Research
1987 ; 219 : 93 96.
16 Atkins RM, Henderson NJ, Duthie RB. Joint contractures in
hemophilias. Clinical Orthopaedics and Related Research 1987 ; 219 :
97 1066.
17 ODwyer NJ, Ada L, Neilson PD. Spasticity and Muscle Contracture Following Stroke. Brain 1996 ; 119 : 1737 1749.
18 Swinyard CA, Bleck EE. The Etiology of Arthorogryposis (Multiple
Congential Contracture). Clinical Orthopaedics and Related Research 1985 ; 194 : 15 29.
19 Akeson WH, Ameil D, Abel MF, Gar n SR, Woo SL-Y. Eects of
Immobilisation on Joints. Clinical Orthopaedics and Related Research 1987 ; 219 : 28 37.
20 Tardieu, C., Tabary, JC., Tardieu, G. and Tabary, C. Adaptation
of Sarcomere Numbers to the Length Imposed on the Muscle.
Advances in Physiological Science 1980 ; 24 : 99 114.
21 Akeson WH, Ameil D, Woo S. Immobility eects on synovial
joints: The pathomechanics of joint contracture. Biorheology 1980 ;
17 : 95 110.
22 Williams PE, Catanese T, Lucey E, Goldspink G. The importance
of stretch and contractile activity in the prevention of connective
tissue accumulation in muscle. Journal of Anatomy 1988 ; 158 :
109 114.
23 McDonald CM. Limb Contractures in Progressive Neuromuscular
disease and the role of Stretching, Orthotics and Surgery. Physical
Medicine and Rehabilitation Clinics of North America 1998 ; 9 :
187 211.
24 McComas AJ. Loss of Muscle Innervation. In : Skeletal Muscle :
Form and Function. Champaign IL: Human Kinetics 1996 ; 251 254.
25 Goldspink G, Tabary C, Tabary JC, Tardieu C, Tardieu G. Eect
of denervation on the adaptation of sarcomeree number and muscle
extensibility on the functional length of muscle. Journal of
Physiology 1974 ; 236 : 733 724.
26 Huet de la Tour E, Tardieu C, Tabary JC, Tabary C. Decrease of
muscle extensibility and reduction of sarcomere number in soleus
muscle following a local injection of tetanus toxin. Journal of
Neurological Science 1979a ; 40 : 123 131.
27 Carey JR, Burghardt T P. Movement dysfunction following central
nervous system lesions : A problem of neurological or muscular
impairment ? Physical Therapy 1993 ; 73 : 538 547.

28 Tardieu C, Huet delaTour E, Bret MD, Tardieu G. Muscle

Hypoextensibility in Children with Cerebral Palsy : I. Clinical and
experimental Observations. Archives of Physical Medicine and
Rehabilitation 1982 ; 63 : 97 102.
29 Alter MJ. Mechanical and Dynamic Properties of Soft tissues. In :
Science of Flexibility Second Edition Leeds: Human Kinetics 1996 ;
59 70.
30 Lehmann JF, Mascock A J, Warren CG, Koblanski J N. Eect of
therapeutic temperature on tendon extensilbility. Archives of
Physical Medicine and Rehabilitation 1970 ; 51 : 481 487.
31 Warren GC, Lehmann JF, Koblanski JN. Heat and Stretch
Procedures :An evaluation using rat tail tendon. Archives of Physical
Medicine and Rehabilitation 1976 ; 57 : 122 126.
32 Ada L, Canning C and Paratz J. Care of the Unconcious HeadInjured Patient. In : L Ada & C Canning (Eds) Key Issues in
Neurological Physiotherap y. Oxford Butterworth Heinmann 1990 ;
249 286.
33 Williams PE. Use of intermittent stretch in the prevention of serial
sarcomere loss in immobilised muscle. Annuals of Rheumatic
Diseases 1990 ; 49 : 316 317.
34 Tardieu C, Lespargot A, Tabary C, Bret MD. For How Long Must
The Soleus Muscle Be Stretched Each Day To Prevent Contracture ?
Developmental Medicine and Child Neurology 1988 ; 30 : 3 10.
35 Worland RL, Arredondo J, Angles F, Lopez-Jimenez F , Jessup
DE. Home continuous passive motion machine versus professional
physical therapy following total knee replacement. Journal of
Arthroplasty 1998 ; 13 : 784 787.
36 Ververeli PA, Sutton DC, Hearn SL, Booth RE Jr, Hozack WJ, Rot
RR. Continuous passive motion after total knee arthroplasty.
Analysis of costs and bene ts. Clinical Orthopaedics and Related
Research 1995 ; 321 : 208 215.
37 Pope DO, Corcoran S, McCaul K, Howie D W. Continuous passive
motion after primary total knee arthroplasty. Journal of Bone and
Joint Surgery (British) 1997 ; 79 : 914 917.
38 Ippolito E, Formisano R, Farsetti R, Caterini, R, Penta F. Excision
for the treatment of periarticular ossi cation of the knee in patients
who have traumatic brain injury. Journa l of Bone and Joint Surgery
(American) 1999 ; 81 : 783 789.
39 Ippolito E, Formisano R, Caterini, R, Farsetti P, Penta F. Resection
of elbow ossi cation and continuous passive motion in postcomatose patients. Journal of Hand Surgery (American) 1999 ; 24 :
546 553.
40 Booth BJ, Doyle M, Montgomery J. Serial Casting For The
Management of Spasticity in the Head-Injured Adult. Physical
Therapy, 1983 ; 63 : 1960 1966.
41 Hoer MM,. Knoebel RT and Roberts R Contractures in cerebral
palsy. Clinical Orthopaedics and Related Research 1987 ; 219 : 70 77.
42 Cusick BD. Serial casts-an approach to Management of static soft
tissue contracture. In : Progressive casting and splinting for Lower
Extremity Deformities in Children with Neuromotor Dysfunction
Tucson, Arizona Therapy Skill Builders, 1990 ; 265 311.
43 Brouwer B, Wheeldon RK, Stradiotto-Parker N, Allum J. Re ex
excitability and isometric force production in cerbral palsy.
Developmental Medicine and Child Neurology 1998 ; 40 : 168 175.
44 Cottalorda J, Gautheron V, Metton G, Charmet E, Chavier Y. Toe
walking in children younger than six years with cerebral palsy The
contribution of Serial Corrective Casts. Journal of Bone & Joint
Surgery (British) 2000 ; 82 : 541 544.
45 Tardieu G, Tardieu C. Cerebral Palsy : Mechanical Evaluation and
Conservative Correction of Limb Joint Contractures. Clinical
Orthopaedics and Related Research 1987 ; 219 : 63 69.
46 Becker AH. Splinting to Prevent Knee Flexion Contractures.
Physical Therapy 1977 ; 57 : 1396.
47 Anderson JP, Snow B, Dorey FJ, Kabo JM. E cacy of Soft Splints
in Reducing Severe Knee Flexion Contractures. Developmental
Medicine and Child Neurology 1988 ; 30 : 502 508.
48 Bonutti PM, Windau JE, Ables BA, Miller BG. Static Progressive
Stretch to Reestablish Elbow Range of Motion. Clinical Orthopaedics and Related Research 1994 ; 303 : 128 134.

557

Disabil Rehabil Downloaded from informahealthcare.com by University of Sussex Library on 10/12/12

For personal use only.

S. E. Farmer and M. James

49 Gelinas JJ, Faber KJ, Patterson SD, King GJW. The eectiveness
of turnbuckle splinting for elbow contracture. Journal of Bone and
Joint Surgery (British) 2000 ; 82 : 74 78.
50 Steen TM, Mollinger LA. Low-load, Prolonged stretch in the
Treatment of Knee Flexion Contractures in Nursing Home
Residents. Physical Therapy 1995 ; 75 : 886 897.
51 Moore P, Major R, Stallard J, Butler PB. ContrActure Correction
Device for Arthrogryposis. Physiotherapy 1990 ; 76 : 303 305.
52 Keeping P, Major R. Use of a Gas Spring Contracture Correction
Orthosis for the Management of a Fixed Flexion Contracture of the
Elbow. Prosthetics and Orthotics Internationa l 1999 ; 23 : 82 84.
53 Charlton P, Ferguson D, Peacock C, Stallard J. Preliminary
Clinical Experience of a Contracture Correction Device. Prosthetics
and Orthotics International 1999 ; 23 : 163 168.
54 James M, Farmer S, Hunt K and Stallard J Contracture Correction
Using Mechanically Applied Torques : A Report to the NHS
Management Executive by Orthotic Research and Locomotor
Assessment Unit, Oswestry, Shropshire and The Centre for Health
Planning and Management, Keele University, Staordshire 1997 ;
23 27.
55 Goldspink DF, Goldspink G. The role of passive stretch in
retarding muscle atrophy In : WA Nix and G Vrbova (Eds)
Electrical stimulation and Neuromuscular Disorders. Heidelberg :
Springer Verlag, 1986 ; 91 100.
56 Pandyan AD, Granat MH. Eects of electrical stimulation on
exion contractures of the hemiplegic wrist. Clinical Rehabilitation
1997 ; 11 : 123 130.
57 Pape KE, Kirsch SE, Galil A, Boulton JE, White MA, Chipman M.
Neuromuscular Approach to Motor de cits of Cerebral Palsy.
Journa l of Pediatric Orthopaedics 1993 ; 13 : 628 633.
58 Gibson JNA, Smith K and Rennie MJ, Prevention of Disuse
Muscle Atrophy by Means of Electrical Stimulation : Maintenance
of Protein Synthesis. The Lancet 1988 ii; 1 October 767 769.
59 Cosgrove AP, Graham HK. Botulinum toxin prevents the development of contracture in hereditary spastic mouse. Developmental
Medicine and Child Neurology 1994 ; 36 : 376 385.
60 Cosgrove AP, Corry IS, Graham HK. Botulinum Toxin in the
Management of the Lower Limb in Cerebral Palsy. Developmental
Medicine and Child Neurology 1994 ; 36 : 386 396.
61 Thompson NS, Baker RJ, Cosgrove AP, Corry IS, Graham HK.
Musculoskeletal modelling in determining the eect of botulinum
toxin on the hamstings of patients with crouch gait. Developmental
Medicine and Child Neurology 1998 ; 40 : 622 625.
62 Boyd R, Graham HK. Botulinum Toxin A in the management of
children with cerebral palsy : indications and outcome. European
Journa l of Neurology 1997 ; 4 : 15 22.
63 Eames NW, Baker R, Hill N, Graham HK. Taylor T, Cosgrove A.
The eect of botulinum toxin A on gastrocnemius length :

558

64
65
66
67
68
69
70

71
72
73
74
75
76
77
78
79

magnitude and duration of response. Developmental Medicine and

Child Neurology 1999 ; 41 : 226 232.
Bleck EE. Orthopaedic Management of Cerebral Palsy. Clinics in
Developmental Medicine 99} 100. London : MacKeith Press, 1987.
Dhawlikar SH, Root L, Mann RL. Distal Lengthening of the
Hamstrings in Patients who have Cerebral Palsy. Journal of Bone
and Joint Surgery 1992 ; 74 : 1385 1391.
Damron TA, Breed AL, Cook T. Diminimished Knee Flexion After
Hamstring Surgery in Cerebral Palsy Patient : Prevalence & Severity.
Journa l of Pediatric Orthopaedics 1993 ; 13 : 188 191.
Sutherland DH, Cooper AS. The Pathomechanics of Progressive
Crouch Gait in Spastic Diplegia. Orthopedic Clinics of North
America 1978 ; 9 : 143 154.
Truscelli D, Lesparot A, Tardieu G. Variation in the Long term
Results of the Tendo Achilles in Children with Cerebral palsy.
Journa l of Bone and Joint Surgery 1979 ; 61 : 466 469.
Abel MF, Damiano DL, Pannunzio M, Bush J. Muscle Ttendon
surgery in diplegic cerebral palsy : functional and mechanical
changes. Journal of Pediatric Orthopaedics 1999 ; 19 : 366 375.
Hoer MM, Barakat G, Koman M. 10 year follow up of split
anterior tibial tendon transfer in cerebral palsied patients with
spastic equinovarus deformity. Journal of Pediatric Orthopaedics
1985 ; 65 : 755 759.
Baker JH, Hall-Craggs EC. Changes in length of sarcomeres
following tenotmy of rat soleus. The Anatomical Record 1987 ; 192 :
55 58.
Tardieu G, Thilleux G, Tardieu C, Huet de la Tour E. Long term
Eects of surgical Lengthening of tendo calcaneus in normal cat.
Developmental Medicine and Child Neurology 1979 ; 21 : 83 94.
Delp SL, Zajac FE. Force and Moment Generating Capacity of
Lower limb Muscles Before and After Tendon Lengthening. Clinical
Orthopaedics and Related Research 1992 ; 284 : 247 259.
Damiano DL, Abel MF, Panninzio M, Romano J-P. Interrelationships of Strength and Gait Before and After Hamstring
Lengthening. Journa l of Pediatric Orthopaedic 1999 ; 19 : 352 358.
Gage JR, Renshaw TS. Gait Analysis : Principles and Applications.
Bone and Joint Surgery 1995 ; 77 : 1607 1623.
Leiber RL. Skeletal Muscle Adaptability 1 : Review of Basic
Properties. Developmental Medicine and Child Neurology 1986 ; 28 :
390 397.
Gordon AM, Huxley AF, Julian FJ. The variations in isometric
tension with sarcomere length in vertebrate muscle bres. Journal of
Physiology 1966 ; 184 : 170 192.
Patrick JH. Techniques of psoas tentomy and rectus transfer:
`New operations for cerebral palsy diplegia. A description. Journal
of Pediatric Orthopaedics Part B 1996 ; 5 : 242 246.
Saraph V, Zwick EB, Uitz C, Linhart W, Steinwender G. The
Baumann procedure for xed contracture of the gastrosoleus in
cerebral palsy. Evaluation of function of the ankle after multilevel
surgery. Journal of Bone Joint Surgery (British) 2000 ; 82 : 535 540.