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REVIEW
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
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-
Disability and Rehabilitatio n ISSN 0963 8288 print} ISSN 1464 5165 online
http:} } www.tandf.co.uk} journals
DOI: 10.108 0} 09638280010029930
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.# #
in c r e a s e d m u s c l e s t if f n e s s
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
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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.
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
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
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
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
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