Acta Orthop Traumatol Turc 2009;43(2):113-120
Treatment approaches to flexion contractures of the knee
Diz fleksiyon kontraktüründe tedavi yaklaşımları
Yener TEMELLİ, N. Ekin AKALAN1
Beyin felcinde en çok etkilenen eklem diz eklemidir.
Diz fleksiyon kontraktürü, çömelme pozisyonunda yü-
rümeye, basma fazında stabilite kaybına, ayakta durma
ve oturmada ve günlük yaşam aktivitelerinde zorluklara
yol açar. Ayrıca, genç erişkin dönemde, patella alta, pa-
tellofemoral eklem dejenerasyonu, patella ve tüberküler
kırıklarına da neden olabilir. Bu çocuklar ileri yaşlarda,
yüksek enerji gerektirdiği için yürümeden bile vazgeçe-
bilirler. Bu yazıda, beyin felçli çocuklarda diz fleksiyon
kontraktürlerinin nedenleri, klinik ve radyolojik değer-
lendirmeler ve tedavi prensipleri gözden geçirildi. Ayrı-
ca, yapılan çalışmalar ve yürüme analizi verileri ışığında
diz fleksiyon kontraktürünün biyomekaniksel nedenleri
ayrıntılı olarak tartışıldı.
Anahtar sözcükler: Beyin felci; çocuk; kontraktür; yürüyüş;
kalça eklemi; diz eklemi; kas, iskelet; tendon.
The knee is the most affected joint in children with cere-
bral palsy. Flexion contracture of the knee is the cause of
crouch gait pattern, instability in stance phase of gait, and
difficulties during standing and sitting, and for daily living
activities. It may also cause patella alta, degeneration of the
patellofemoral joint, and stress fractures of the patella and
tibial tubercle in young adults. Children with cerebral palsy
may even give up walking due to its high energy demand
in the adult period. The purpose of this article is to review
the causes of the knee flexion contractures, clinical and ra-
diological evaluations, and treatment principles in children
with cerebral palsy. The biomechanical reasons of knee
flexion deformity are discussed in detail in the light of pre-
vious studies and gait analysis data.
Key words: Cerebral palsy; child; contracture; gait; hip joint;
knee joint; muscle, skeletal; tendons.
Correspondence / Yazışma adresi: Dr. Yener Temelli. İstanbul Tıp Fakültesi, Ortopedi ve Travmatoloji Anabilim Dalı, 34093 Çapa, İstanbul, Turkey.
Tel: +90 212 - 414 20 00 / 32535 e-mail: email@example.com
Submitted / Başvuru tarihi: 16.01.2009 Accepted / Kabul tarihi: 10.03.2009
©2009 Turkish Association of Orthopaedics and Traumatology / ©2009 Türk Ortopedi ve Travmatoloji Derneği
Departments of Orthopedics and Traumatology and 1Child Neurology, Medicine Faculty of İstanbul University, İstanbul
Hamstring spasticity is the most common problem in
cerebral palsy (CP). If left untreated, it results in knee
flexion contractures. Untreated flexion contractures
lead to gradual deformation of the femoral condyles.
In literature, crouch gait is reported in 69% of the
general CP population, being 74% in diparetic and
88% in quadriparetic patients.
Knee flexion contracture in children with CP
causes crouch gait and excessive energy consump-
tion during walking, making daily activities difficult
such as standing, reaching to objects, and standing up
from a chair. Quadriceps muscle works excessively
as a result of knee flexion contracture. This increases
the loading on several joints, especially on the patel-
lofemoral joint and becomes an important problem
causing anterior knee pain and stress fractures of the
patella and tibial tubercle.[3-5]
Together with other common neuromuscular and
musculoskeletal problems in CP patients, knee flex-
ion contracture makes functional activities more dif-
ficult. A detailed evaluation is necessary to decide the
The aim of this article is to assess the reasons of
knee flexion contractures in children with CP, ana-
lyze assessment methods, overview compensatory
mechanisms related to deformities, and discuss treat-
114 Acta Orthop Traumatol Turc
Fig. 1. Location of the ground reaction force (GRF) in
ment alternatives for detected problems for selecting
the most appropriate treatment for the patient.
Causes of knee flexion contracture
Knee flexion contracture may develop (i) after hip
flexion contracture and increased anterior pelvic tilt,
or due to (ii) hamstring spasticity or contracture, (iii)
gastrocnemius tightness, (iv) triceps surae weakness
following surgery, or (v) posterior capsule contracture
that develop over time.[6-10]
Hamstring spasticity or contractures
Medial and lateral hamstrings attached to the
proximal tibia are knee flexors and hip exten-
sors. Three-dimensional gait analysis studies
showed prolonged medial hamstring muscle ac-
tivity resulting in increased hip extensor muscle
strength. It has long been believed that children
with crouch gait have hamstring spasticity and this
has been the focus of several studies. Many have
shown that hamstring lengths are usually normal in
these children.[5,6,9,12] Even though the length of the
hamstring is normal, it appears contracted when
pelvic tilt increases. Hamstring release in this con-
dition will further increase the pelvic tilt. Thus,
decision for hamstring release operation should be
made after clinical tests and three-dimensional gait
analysis which provides dynamic length measure-
ment of hamstring muscles.[5,9,12,13]
Long-standing knee flexion contracture imposes a
heavy burden on knee extensor muscles that results in
patella alta. This makes knee extension by quadriceps
difficult during the stance phase. Therefore, no matter
how effective knee extensors are, the lever arm of the
knee will not be sufficient for full knee extension. In
severe cases, this condition gives rise to patella and
tibial tubercle fractures.
Knee flexion contracture following
hip flexion contracture and
increased anterior pelvic tilt
Anterior pelvic tilt and knee flexion are usually in-
creased in children with CP while standing or dur-
ing the stance phase of gait.[5,7,9,13] Normally, ground
reaction force (GRF) passes from the center of the
hip and knee while standing. In children with crouch
gait, the GRF passes from anterior of the hip and pos-
terior of the knee because of hip flexor tightness (Fig.
1). Lumbar lordosis is increased. To compensate lum-
bar lordosis, superior part of the trunk moves back
and the knee is flexed. This crouching posture at
the hip and knee leads to knee flexion contracture
over time. Increased knee flexion associated with in-
creased anterior pelvic tilt contributes to knee flexion
contracture in time. As anterior pelvic tilt continues
to increase, knee flexion during standing and walking
will increase. Usually this might be perceived as an
increase in knee flexor tightness clinically, necessitat-
ing hamstring lengthening.
The gastrocnemius muscle is the primary ankle plan-
tar flexor and knee flexor. As knee flexion increas-
es, flexion moment of the gastrocnemius at the knee
gradually increases. There is selective motor deficit
in the gastrocnemius muscle of children with CP and
spasticity dominates. For this reason, it is usually
stretched, causing early heel rise, toe walking, and
heel valgus during the stance phase of gait. Gas-
trocnemius causes toe walking distally and this forms
an extra proximal moment pulling the knee to flex-
ion. This moment directly affects acceleration of
the knee to flexion at the end of the stance phase and
contributes to maximum flexion of the knee during
Temelli and Akalan. Treatment approaches to flexion contractures of the knee
the swing phase. Gastrocnemius-soleus complex is
the most important part of plantar flexion-knee ex-
tension couple which provides adequate knee exten-
sion during the stance phase. While gastrocnemius
muscle stretch occurring in the proximal contributes
to increased knee flexion, it loses its important role
in extension during the stance phase and becomes a
Postoperative triceps surae weakness
Soleus generates 40% to 50% of the total force
needed to straighten the body during the first one-
third of gait cycle. This activity enables knee flex-
ion by producing a moment against the GRF passing
from the anterior of the ankle. This plantar flexor
effect on the ankle and extensor effect on the knee is
called plantar flexion-knee extension couple. Thus,
extra muscle activation for knee extension during
the stance phase is eliminated. In spastic diplegia
and quadriplegia, the gastrocnemius and hip flexor
muscles stretch while the soleus, vastus muscles,
and gluteus maximus elongate. Any procedure that
weakens the soleus such as selective dorsal rhizo-
tomy or Achilles tendon release results in deficiency
of the soleus to retract the tibia. As a result, ankle
dorsiflexion and knee flexion increase during the
stance phase, leading to the crouch gait pattern and
knee flexion contracture.
Posterior knee capsule tightness
Knee flexion contracture leads to shortening and
thickening of the posterior capsule and shortening
of the sciatic nerve. For this reason, particularly in
fixed knee contractures of 30° to 40°, it is suggested
that hamstring release be combined with posterior
Assessment methods of
knee flexion contracture
Knee flexion contractures are assessed clinically and
by laboratory and imaging studies.
Clinical assessment methods
Patients on their mothers’ lap or walking with the
help of an assistive device (walker, canadian crutch,
cane) should be observed for lower extremity position
and activity. Posterior pelvic tilt, lumbar kyphosis and
forward bending of the trunk while sitting give clues
about possible hamstring contracture and/or trunk
In order to determine the underlying cause of
knee flexion contracture, hamstring muscles should
first be assessed. The popliteal angle never exceeds
50° throughout the life. However, it may increase
up to 90° in CP. Thus, in the first instance, the
popliteal angle and hamstring contracture should
be assessed (Fig. 2). During this test, the physician
observes whether hamstring spasticity and dynamic
contracture are present by increasing the speed of
passive knee extension. Measurement of the ham-
string length is important to distinguish between
normal and contracted muscle lengths (Fig. 2b). The
popliteal angle is measured both unilaterally and bi-
laterally. Hamstring shift is calculated by subtract-
ing unilateral popliteal angle from bilateral popliteal
angle (Fig. 2a, b).
Unilateral popliteal angle is measured while the
patient’s existing lumbar lordosis is preserved and
the contralateral hip is in neutral position. It gives
information on functional hamstring contracture.
However, bilateral popliteal angle is measured by
Fig. 2. Determination of the (a) popliteal angel and (b) hamstring shift.
116 Acta Orthop Traumatol Turc
Fig. 3. (a) Increased internal rotation and (b) decreased external rotation of the hip in femoral anteversion.
bringing the contralateral hip to flexion until the
ASIS (anterior superior iliac spine) and PSIS (pos-
terior superior iliac spine) are vertical. Then, ipsi-
lateral popliteal angle is measured, which provides
information about true hamstring contracture (Fig.
2b). The difference between the two angles shows if
hamstring length is normal or not. If the difference
is greater than normal, this means that hamstring
tightness decreases with posterior rotation of the
pelvis, suggesting normal hamstring length. In gen-
eral, anterior pelvic tilt is increased in patients with
spastic diparesia and quadriparesia, with a greater
hamstring shift. If the clinician determines func-
tional hamstring contracture without bringing pelvic
tilt to normal and performs hamstring release, this
will further decrease hip extensor moment of ham-
strings, increase pelvic tilt, and as a result of con-
tracted hip flexors, end up with knee flexion during
gait.[10,13,17] Delp et al. found that every 1° increase
in pelvic anterior tilt increased bilateral popliteal
angle by 2°. Thus, a difference of greater than 20°
between unilateral and bilateral popliteal angles of-
ten suggests hip flexor contracture, weak abdominal
muscles and/or weak hip extensor muscles. Consid-
ering the difficulties in clinical measurement of dy-
namic hamstring length, evaluation of the patient in
gait analysis laboratory is necessary.
Clinically gastrocnemius-soles tightness should
be assessed separately like the hamstring muscles,
because the soleus muscle is usually normal or ex-
tended in most CP patients. The primary role of the
soleus is to control the forward movement of the tibia
during the mid-stance phase, thereby enabling knee
extension. Radical soleus stretching exercises and
surgical procedures such as Achilles tendon release
that cause excessive lengthening of the soleus weak-
ens the muscle, resulting in increased knee flexion
during the stance phase and knee flexion contracture.
The Silfverskiöld test performed under anesthesia is
the most appropriate method to identify gastrocne-
mius contracture and excessive soleus length. But, the
positioning of the mid and front segments of the feet
should not interfere with the test. Thus, the subtalar
joint is brought to as much neutral or varus position
as possible during the test.
Delay in walking and hip flexion cause high femo-
ral anteversion in children with CP. With increased
anteversion, the child walks in internal rotation and
pelvic tilt increases. Increased femoral anteversion is
associated with kinetic and kinematic changes that
result in crouch posture. Therefore, correction of ro-
tational deformities is first line treatment of crouch
posture in CP patients if orthopedic procedures are
considered (Fig. 3).
Clinically video-based observational gait analy-
sis (VBOGA) may help understand the influence of
knee flexion contracture on walking. The clinical
application of this method can be made by a sin-
gle specialist experienced in VBOGA. It has been
shown that observation of the gait in slow motion
and evaluation of the gait in fewer phases (dividing
the stance phase to three parts only) with a simple
evaluation form increase reliability.[18,19] Even though
Temelli and Akalan. Treatment approaches to flexion contractures of the knee
detailed and time consuming, Perry’s observational
gait analysis evaluation form developed in 1992 is
still used for gait assessment.[3,19]
Computerized gait analysis
In CP patients with knee contracture, kinetic analy-
sis of gait shows increased knee flexion in the stance
phase and, despite minimal movement of the knee in
the swing phase, an increase in the knee extensor mo-
ment during the loading phase, and increased quad-
riceps activity, depending on the severity of contrac-
ture. This is because the extensor muscles are trying
to bring the knee to extension. Knee flexion con-
tracture is not examined in the laboratory solely in
the knee context, investigation of its effects on other
joints is helpful for the treatment.
In spastic diplegia and quadriplegia, usually
crouch gait is seen (Fig. 4). Foot dorsiflexion and
knee flexion are increased due to soleus weakness
and/or femoral anteversion and there is a continuous
increase in the knee extensor moment. EMG shows
increased hip and knee extensor muscle activity and
high energy consumption. With addition of ankle
plantar flexion during the stance phase to this pic-
ture, the knee is flexed in the beginning of the stance
Management of knee flexion deformities
The goals of treatment should be as follows:
1. Decrease knee flexion during gait,
2. Increase stride length,
3. Decrease patellofemoral joint load, and
4. Increase strength (durability).
In principle, the pelvis, hip, knee, and ankle should be
assessed as a whole.
1. Rotational deformities (femoral anteversion,
tibial torsion, varus-valgus-adductus deformi-
ties of the feet, hip subluxation, etc.) should be
2. Shortened muscles should be lengthened (care
should be given to biarticular muscles).
3. Elongated muscles should be shortened.
Fig. 4. (a) Crouch gait with increased hip and knee flexion, anterior pelvic tilt, and ankle dorsiflex-
ion (preoperative). (b) Gait is close to normal (postoperative).
118 Acta Orthop Traumatol Turc
Fig. 5. Preoperative and postoperative images of a patient undergoing supracondylar femoral osteotomy and patellar
4. Fixed joint contractures should be corrected.
5. Ground reaction orthosis may be needed.
In mild knee flexion contractures, immobilizer, an-
gle adjustable KAFO, and botulinum toxin A injec-
tion can be used in children younger than 5 years age
whose popliteal angle is smaller than 60 degrees.
Botulinum toxin A injection should be used in
carefully selected patients. Corry et al. showed that
anterior pelvic tilt increased after botulinum toxin A
injection to hamstring muscles in 10 CP patients with
crouch gait. Care should be taken not to cause iso-
lated hamstring weakness. As the hamstring is a hip
extensor, its excessive weakness increases anterior
If knee flexion contracture is between 10 to 30 de-
grees, surgery is necessary in patients older than 10
years. Hamstring lengthening and if necessary poste-
rior knee capsulotomy operations can be performed.
Gradual correction with casting may be rarely nec-
essary. No deformity has developed in femoral con-
Indications of hamstring lengthening
1. Popliteal angle is greater than 50° under an-
esthesia and knee flexion is greater than 20°
2. Fixed knee contracture is greater than 5°-10°,
3. Having difficulty sitting and standing without a
4. Disappearance of lumbar kyphosis while sit-
ting with hamstring relaxation.
Semitendinosus, semimembranosus, and long head
of the biceps femoris are knee flexors and hip exten-
sors. Semitendinosus and semimembranosus length-
ening may correct the popliteal angle separately by
10 to 15 degrees. Excessive hamstring lengthening
should be avoided because it causes anterior pelvic
tilt and stiff knee gait. If the biceps femoris is not
lengthened intramuscularly, it may lead to tibial ex-
Should we use passive hamstring stretching?
Instead of long-term aggressive hamstring stretch
exercises, functional stretching and relaxation meth-
ods can be more effective in relaxing the child’s tight
muscles and whole body during play.
If fixed knee flexion contracture is greater than
30°, the distal ends of the femoral condyles may
become flattened, disrupting the articular surface
of the tibiofemoral joint. In this situation, distal
femoral extension osteotomy is a better option than
capsular release. Capsular release in the presence
of flattened femoral condyles results in decreased
slide/roll behavior of the tibiofemoral joint, turning
the knee joint a hinge joint rather than a sliding one
around the condyles. Hamstring lengthening, patel-
lar tendon plication, and distal tibial tubercle transfer
may be performed in the same session after supra-
condylar osteotomy. Since distal femoral extension
will cause femoral shortening, the development of
sciatic nerve palsy will be much rarer. Supracondy-
lar closing wedge extension osteotomy of the femur
is an effective and safe procedure for the correction
of knee flexion contracture in adult patients with
spastic diparesis. One advantage of this operation
is femoral shortening and relief of neurovascular
structures. Sciatic nerve neuropathy and vascular
insufficiency are rare (Fig. 5).
Temporary growth arrest of anterior femoral epi-
physis is a new method used in the management of
knee flexion contractures (Fig. 6). This method
should be used in patients around 13 years of age,
Temelli and Akalan. Treatment approaches to flexion contractures of the knee
with 5 to 20 degrees of flexion contracture. Genu re-
curvatum deformity develops in patients less than 13
years of age and deformity correction is incomplete
in patients older than 14 years.
Results and problems
Potential problems related to treatment include:
1. Recurrence of knee flexion deformity.
2. Increases in postoperative lumbar lordosis and
anterior pelvic tilt should be avoided. If pres-
ent, hip flexion contracture should also be cor-
3. In the presence of quadriceps spasticity or if
the hamstrings are too weak, stiff knee gait or
genu recurvatum will ensue. Distal rectus fem-
oris transfer will solve the problem.
4. Partial correction of knee flexion deformity.
5. Crouch gait may develop due to excessive tri-
ceps lengthening. Solution is ground reaction
6. Sciatic nerve lesion.
As a principle, the pelvis, hip, knee, and ankle
should be assessed as a whole. Rotational deformities
should be corrected initially. Muscle length should
be balanced, fixed joint contractures should be cor-
rected, and recurrence of fixed contractures should be
avoided by using ground reaction orthoses.
1. Freeman M. Gait. In: Cerebral palsy. New York: Springer;
2005. p. 251-386.
2. Wren TA, Rethlefsen S, Kay RM. Prevalence of specific
gait abnormalities in children with cerebral palsy: influ-
ence of cerebral palsy subtype, age, and previous surgery. J
Pediatr Orthop 2005;25:79-83.
3. Sutherland DH, Davids JR. Common gait abnormali-
ties of the knee in cerebral palsy. Clin Orthop Relat Res
4. Topoleski TA, Kurtz CA, Grogan DP. Radiographic abnor-
malities and clinical symptoms associated with patella alta
in ambulatory children with cerebral palsy. J Pediatr Or-
5. Gage JR. Treatment principles for crouch gait. In: Gage JR,
editor. The treatment of gait problems in cerebral palsy.
London: Mac Keith Press; 2004. p. 382-97.
6. Arnold AS, Anderson FC, Pandy MG, Delp SL. Muscu-
lar contributions to hip and knee extension during the
single limb stance phase of normal gait: a framework for
investigating the causes of crouch gait. J Biomech 2005;
7. Ounpuu S, Gage JR, Davis RB. Three-dimensional lower
extremity joint kinetics in normal pediatric gait. J Pediatr
8. Kirtley C. Support and forward progression. In: Clinical
gait analysis: theory and practice. London: Churchill Liv-
ingstone; 2006. p. 237-54.
9. Horstmann HM, Bleck EE. Knee. In: Orthopaedic manage-
ment in serebral palsy. 2nd ed. London: Mac Keith Press;
2007. p. 303-43.
10. Trost J. Physical assessment and observational gait analy-
sis. In: Gage JR, editor. The treatment of gait problems in
cerebral palsy. London: Mac Keith Press; 2004. p. 71-89.
11. Waters RL, Perry J, McDaniels JM, House K. The relative
strength of the hamstrings during hip extension. J Bone
Joint Surg [Am] 1974;56:1592-7.
12. Arnold AS, Liu MQ, Schwartz MH, Ounpuu S, Delp SL.
The role of estimating muscle-tendon lengths and veloci-
ties of the hamstrings in the evaluation and treatment of
crouch gait. Gait Posture 2006;23:273-81.
13. Delp SL, Arnold AS, Speers RA, Moore CA. Hamstrings and
psoas lengths during normal and crouch gait: implications for
muscle-tendon surgery. J Orthop Res 1996;14:144-51.
14. Goldberg SR, Anderson FC, Pandy MG, Delp SL. Muscles
that influence knee flexion velocity in double support: im-
plications for stiff-knee gait. J Biomech 2004;37:1189-96.
15. Seth A, Liu MQ, Schwartz MH, Anderson FC, Delp SL. Treat-
ment insight from subject-based simulation of crouch gait. In:
North American Congress on Biomechanics (NACOB); Au-
gust 5-9, 2008; Ann Arbor, Michigan, USA. No: 543.
16. Acevedo JS. The infant and child with cerebral palsy. In:
Tecklin JS, editor. Pediatric physical therapy. 4th ed. Phila-
delphia: Lippincott Williams & Wilkins; 2007. p. 179-253.
17. Schutte LM, Hayden SW, Gage JR. Lengths of hamstrings
and psoas muscles during crouch gait: effects of femoral
anteversion. J Orthop Res 1997;15:615-21.
18. Akalan NE. Serebral parezili çocuklarda video bazlı gö-
zlemsel yürüme analizinin gözlemci içi ve gözlemciler arası
Fig. 6. Temporary growth arrest of anterior femoral epi-
120 Acta Orthop Traumatol Turc Download full-text
güvenilirliğinin belirlenmesi [Yüksek lisans Tezi]. İstanbul:
İstanbul Üniversitesi Sağlık Bilimleri Enstitüsü; 1999.
19. Krebs DE, Edelstein JE, Fishman S. Reliability of ob-
servational kinematic gait analysis. Phys Ther 1985;65:
20. Corry IS, Cosgrove AP, Duffy CM, Taylor TC, Graham
HK. Botulinum toxin A in hamstring spasticity. Gait Pos-
21. Halbertsma JP, Göeken LN. Stretching exercises: ef-
fect on passive extensibility and stiffness in short ham-
strings of healthy subjects. Arch Phys Med Rehabil 1994;