Cerebral Palsy – An Orthopaedic Overview

Cerebral palsy (CP) is a group of permanent disorders of movement and posture caused by a non-progressive disturbance of the developing fetal or infant brain. Although the primary neurological lesion is non-progressive, the resulting musculoskeletal deformities may progress with growth.

From an orthopaedic perspective, the major problems in cerebral palsy arise from abnormal muscle tone, muscle imbalance, weakness, impaired selective motor control, contractures, altered growth and progressive skeletal deformity.

Orthopaedic management therefore aims not simply to correct deformity, but to improve or preserve mobility, sitting balance, hygiene, comfort, positioning and overall quality of life.

The brain injury in cerebral palsy does not worsen with time, but the musculoskeletal consequences can become progressively more severe as the child grows.

Persistent muscle imbalance and abnormal tone may initially produce a dynamic deformity. With time, muscle-tendon shortening, capsular contracture, torsional abnormalities and bony deformity may develop.

Dynamic deformity may eventually become fixed deformity.

Cerebral palsy results from injury or abnormal development of the immature brain. The insult may occur prenatally, perinatally or postnatally.

• Prematurity.
• Periventricular leukomalacia.
• Intraventricular haemorrhage.
• Hypoxic-ischaemic brain injury.
• Congenital brain malformations.
• Intrauterine infection.
• Neonatal stroke.
• Severe neonatal infection.
• Postnatal meningitis or encephalitis.
• Traumatic or hypoxic brain injury in infancy.

The exact neurological pattern and functional disability depend on the location and severity of brain involvement.

• Hemiplegia / unilateral CP: predominantly one side of the body is involved, usually with upper limb involvement at least as significant as the lower limb.
• Diplegia: both lower limbs are predominantly affected, with relatively less involvement of the upper limbs.
• Quadriplegia: all four limbs and trunk are significantly involved.

Modern classification increasingly emphasises functional ability rather than relying solely on terms such as diplegia and quadriplegia.

The Gross Motor Function Classification System is one of the most useful systems for describing functional mobility in children with cerebral palsy.

GMFCS level strongly influences orthopaedic goals, hip surveillance strategies and expectations from surgery.

The growing skeleton is continuously exposed to abnormal forces produced by spasticity, muscle imbalance, weakness and impaired motor control.

Important contributors include:

• Spasticity.
• Dystonia.
• Muscle weakness.
• Loss of selective motor control.
• Failure of muscle growth to keep pace with bone growth.
• Muscle-tendon contracture.
• Abnormal joint loading.
• Torsional bone deformity.
• Reduced weight bearing.

Over time, dynamic muscle imbalance can lead to fixed contractures, hip displacement, torsional deformity, foot deformity and spinal deformity.

Distinguishing dynamic spasticity from fixed muscle-tendon contracture is essential before planning orthopaedic treatment.

Assessment should evaluate the entire child rather than focusing on a single joint.

• GMFCS level and mobility.
• Sitting and standing balance.
• Gait pattern.
• Muscle tone and distribution of spasticity.
• Selective motor control.
• Muscle power.
• Passive joint range of motion.
• Fixed contractures.
• Hip stability.
• Femoral and tibial rotational profile.
• Knee flexion and extension.
• Ankle dorsiflexion with knee flexed and extended.
• Foot alignment.
• Spinal alignment.
• Pain, hygiene and positioning difficulty.

Progressive hip displacement is one of the most important orthopaedic complications of cerebral palsy, particularly in children with limited ambulatory ability.

Hip displacement is generally acquired and progressive rather than a true congenital dislocation. It develops because abnormal muscle forces act on a growing proximal femur and acetabulum.

Common contributing factors include:

• Hip adductor spasticity and contracture.
• Hip flexor tightness.
• Weak hip abductors and extensors.
• Persistent femoral anteversion.
• Increased femoral neck-shaft angle.
• Limited weight bearing.

Hip surveillance consists of regular clinical and radiographic assessment designed to detect progressive hip displacement before painful dislocation and severe acetabular deformity develop.

Surveillance intensity is based largely on age, GMFCS level and the degree or progression of hip displacement.

Children at higher GMFCS levels generally have a greater risk of progressive hip displacement and therefore require closer surveillance.

Hip surveillance is one of the most important preventive orthopaedic strategies in cerebral palsy.

Reimers migration percentage is commonly used to quantify lateral displacement of the femoral head on an AP pelvis radiograph.

It represents the percentage of the ossified femoral head lying lateral to the lateral margin of the acetabulum as defined by Perkins line.

A progressively increasing migration percentage indicates worsening lateral displacement and is more clinically important than a single isolated measurement.

Migration percentage above approximately 30% is commonly considered abnormal and warrants close surveillance and orthopaedic assessment.

• Progressive reduction in hip abduction.
• Adductor contracture.
• Pelvic obliquity.
• Difficulty with perineal hygiene.
• Pain during sitting or transfers.
• Deterioration in standing or gait.
• Asymmetric sitting posture.
• Apparent limb-length discrepancy.

Clinical examination alone cannot reliably exclude progressive hip displacement; radiographic surveillance remains essential in at-risk children.

Treatment depends on age, GMFCS level, migration percentage, progression, hip morphology, contracture and symptoms.

Early / Preventive Procedures

• Adductor lengthening or release.
• Iliopsoas lengthening in selected cases.
• Associated tone management.

Soft-tissue surgery may be useful in selected younger children with early displacement, but its ability to prevent progression is limited when substantial structural deformity is already present.

Reconstructive Procedures

• Proximal femoral varus derotation osteotomy.
• Femoral shortening where required.
• Pelvic osteotomy when acetabular dysplasia is significant.
• Open reduction in selected dislocated or severely displaced hips.

Proximal femoral varus derotation osteotomy is one of the key reconstructive procedures for progressive hip displacement in cerebral palsy.

It may address:

• Excessive femoral anteversion.
• Excessive proximal femoral valgus.
• Lateral displacement of the femoral head.
• Excessive soft-tissue tension when combined with shortening.

Pelvic reconstruction may be added when acetabular deficiency is significant.

In a non-ambulatory patient with a longstanding, painful, severely deformed dislocated hip, reconstructive surgery may no longer be appropriate.

The goals then become:

• Pain relief.
• Improved sitting.
• Improved hygiene.
• Reduced care difficulty.

Salvage procedures are individualised and may include proximal femoral resection or other palliative reconstructive procedures in carefully selected patients.

Gait abnormalities in ambulant children with cerebral palsy result from a combination of spasticity, contracture, muscle weakness, torsional deformity and impaired motor control.

Common sagittal-plane gait patterns include:

• True equinus gait.
• Jump gait.
• Apparent equinus gait.
• Crouch gait.

Equinus is one of the commonest lower-limb deformities in cerebral palsy and is usually related to overactivity or contracture of the gastrocnemius-soleus complex.

Patients may demonstrate toe walking, reduced heel contact, instability or abnormal knee mechanics.

The Silfverskiöld test helps differentiate isolated gastrocnemius tightness from combined gastrocnemius-soleus contracture.

Treatment Options

• Physiotherapy and stretching.
• Ankle-foot orthosis.
• Serial casting.
• Botulinum toxin in selected dynamic equinus.
• Gastrocnemius recession.
• Gastrocsoleus lengthening in selected fixed contractures.

Excessive lengthening of the plantar-flexor mechanism should be avoided because it can produce weakness and contribute to crouch gait.

Crouch gait is characterised by excessive hip and knee flexion during stance, often associated with excessive ankle dorsiflexion.

Important contributors include:

• Hamstring contracture.
• Hip flexion contracture.
• Weak plantar flexors.
• Lever-arm dysfunction.
• Excessive femoral anteversion.
• External tibial torsion.
• Patella alta.
• Quadriceps insufficiency.

Crouch gait may progressively increase the energy cost of walking and cause anterior knee pain and functional deterioration.

Treatment should address the specific biomechanical abnormalities identified rather than simply lengthening every apparently tight muscle.

Procedures may include:

• Selective hamstring lengthening in appropriate patients.
• Correction of rotational deformity.
• Correction of foot lever-arm dysfunction.
• Patellar tendon advancement in selected patients.
• Distal femoral extension osteotomy for fixed knee flexion deformity.
• Combined multilevel reconstruction.

Knee problems are common in ambulatory cerebral palsy and frequently contribute to crouch gait.

Common abnormalities include:

• Hamstring spasticity.
• Fixed knee flexion contracture.
• Rectus femoris overactivity causing stiff-knee gait.
• Patella alta.
• Extensor mechanism insufficiency.
• Anterior knee pain.

Stiff-knee gait is characterised by reduced or delayed knee flexion during swing phase.

A common contributor is inappropriate rectus femoris activity during swing.

In selected ambulant patients, rectus femoris transfer may be considered as part of multilevel gait reconstruction.

Torsional deformities are common in cerebral palsy and can impair the effective lever arms of the muscles acting across the hip, knee and ankle.

Femoral Anteversion

Persistent excessive femoral anteversion may produce internal hip rotation and an internally rotated gait.

Tibial Torsion

External tibial torsion is particularly important because it can worsen lever-arm dysfunction and crouch gait.

Symptomatic fixed torsional deformity may require femoral or tibial derotation osteotomy.

Effective walking depends on the skeleton functioning as a series of stable lever arms through which muscles generate movement.

Torsional deformities and unstable foot deformities shorten or redirect these lever arms, reducing the mechanical effectiveness of otherwise functioning muscles.

Weakness in cerebral palsy may therefore be partly functional: correcting skeletal lever arms can improve the effectiveness of existing muscle power.

Foot deformities vary according to age, CP distribution and muscle imbalance.

Common deformities include:

• Equinus.
• Equinovarus.
• Planovalgus.
• Cavovarus in selected hemiplegic patients.
• Hallux valgus.
• Toe deformities.

Equinovarus is seen particularly in unilateral spastic cerebral palsy and results from imbalance between invertors and evertors together with plantar-flexor overactivity.

Dynamic deformity may be treated with orthoses, tone management and selected tendon procedures. Fixed deformity may require tendon lengthening or transfer and, in older children, bony correction.

Procedures may include split posterior tibial tendon transfer or split anterior tibial tendon transfer in carefully selected dynamic deformities.

Planovalgus is common in bilateral cerebral palsy and may progress from a flexible deformity to a painful rigid foot.

Features include:

• Hindfoot valgus.
• Midfoot collapse.
• Forefoot abduction.
• Reduced medial longitudinal arch.
• Prominent talar head.

Treatment ranges from orthoses for flexible deformity to calcaneal lengthening, other reconstructive osteotomies or fusion procedures for selected severe rigid deformities.

Scoliosis is an important problem particularly in children with severe bilateral involvement and reduced ambulatory function.

Neuromuscular scoliosis in cerebral palsy may be long, sweeping and associated with significant pelvic obliquity.

Potential consequences include:

• Poor sitting balance.
• Difficulty with positioning and wheelchair seating.
• Pain.
• Skin pressure problems.
• Progressive pelvic obliquity.
• Respiratory compromise in severe cases.

Early management includes optimising seating, posture and overall medical status. Bracing may help positioning or sitting support but generally has limited ability to prevent progression of a major neuromuscular scoliosis.

Progressive severe deformity causing pain, poor sitting balance or major functional difficulty may require spinal fusion.

Surgical decision-making must consider:

• Nutritional status.
• Respiratory function.
• Seizure disorder.
• Bone quality.
• Skin condition.
• Hip status.
• Pelvic obliquity.
• Overall goals of care.

Upper-limb involvement is especially important in hemiplegic and quadriplegic patterns.

Common deformities include:

• Shoulder internal rotation and adduction.
• Elbow flexion contracture.
• Forearm pronation deformity.
• Wrist flexion and ulnar deviation.
• Thumb-in-palm deformity.
• Finger flexion deformity.

The objectives of treatment may include improved hygiene, appearance, bimanual function and hand positioning rather than normalisation of movement.

Spasticity management is multidisciplinary and should be goal-directed.

Options include:

• Physiotherapy.
• Stretching and positioning programmes.
• Orthoses.
• Serial casting.
• Oral antispasticity medication.
• Botulinum toxin injections.
• Intrathecal baclofen in selected severe generalised spasticity.
• Selective dorsal rhizotomy in carefully selected patients.
• Orthopaedic surgery for established structural deformity.

Botulinum toxin reduces excessive activation of selected muscles temporarily by blocking neuromuscular transmission.

It is most useful for dynamic focal spasticity when a fixed structural contracture has not yet become dominant.

Common lower-limb targets include:

• Gastrocnemius.
• Adductors.
• Hamstrings.
• Other selected overactive muscles based on individual goals.

Botulinum toxin does not correct established bony deformity and should not be regarded as a substitute for reconstruction when significant fixed deformity has developed.

Orthoses are commonly used to improve alignment, provide stability, maintain range and optimise gait.

Ankle-foot orthoses may be designed to:

• Control equinus.
• Improve heel contact.
• Improve foot stability.
• Influence knee position during stance through the ankle-foot relationship.
• Reduce energy expenditure in selected gait patterns.

Orthotic prescription should therefore be based on the patient's gait pattern and functional objective rather than simply the presence of spasticity.

Surgery should address structural deformities that limit function or cause pain, instability, positioning problems or hygiene difficulty.

Important principles include:

• Establish realistic functional goals.
• Distinguish dynamic from fixed deformity.
• Analyse the whole limb rather than a single joint.
• Avoid weakening already weak muscle groups unnecessarily.
• Correct lever-arm dysfunction where relevant.
• Preserve useful compensatory mechanisms.
• Coordinate surgery with rehabilitation.

Ambulatory children with cerebral palsy often have abnormalities at several anatomical levels. Correcting only one deformity may fail to improve overall gait and can sometimes expose another previously compensated abnormality.

Single-event multilevel surgery (SEMLS) refers to correction of multiple significant musculoskeletal deformities during a single operative episode followed by coordinated rehabilitation.

Procedures may include combinations of:

• Muscle-tendon lengthening.
• Tendon transfer.
• Femoral derotation osteotomy.
• Tibial derotation osteotomy.
• Foot reconstruction.
• Patellar advancement.
• Distal femoral extension osteotomy.

SEMLS aims to correct the major gait-limiting deformities together rather than performing repeated isolated operations during childhood.

Instrumented three-dimensional gait analysis can help define the interaction between dynamic movement and structural deformity in ambulant children with complex gait abnormalities.

A comprehensive gait laboratory assessment may include:

• Video analysis.
• Kinematics.
• Kinetics.
• Dynamic electromyography.
• Temporal-spatial parameters.
• Energy expenditure assessment in selected settings.

Gait analysis is particularly useful when planning multilevel surgery because clinical examination alone may not reveal the precise contribution of individual muscles and skeletal deformities.

Muscle surgery cannot reliably correct a mature structural bony deformity.

Timing is one of the most challenging aspects of cerebral palsy reconstruction.

Surgery performed too early may be followed by recurrence as the child grows, whereas surgery delayed until severe fixed deformity develops may require larger and more complex reconstruction.

The timing therefore depends on:

• Age.
• Functional level.
• Progression of deformity.
• Presence of pain.
• Gait deterioration.
• Hip migration.
• Degree of fixed contracture.
• Remaining growth.

A procedure that is appropriate for a GMFCS II child may therefore be inappropriate for a GMFCS V child with completely different functional priorities.

Pain should not be assumed to arise purely from spasticity. Orthopaedic causes must be actively sought.

Important causes include:

• Hip subluxation or dislocation.
• Scoliosis.
• Contractures.
• Foot deformity.
• Patellofemoral overload in crouch gait.
• Pressure-related skin problems.
• Occult fractures in children with poor bone density.

Children and adults with severe cerebral palsy may have reduced bone mineral density and increased fracture risk, especially when mobility and weight bearing are limited.

Contributing factors may include:

• Reduced weight bearing.
• Poor nutritional intake.
• Vitamin D deficiency.
• Low muscle mass.
• Use of certain long-term anticonvulsant medications.
• Previous fragility fractures.

Cerebral palsy cannot be managed effectively by orthopaedic surgery alone.

The multidisciplinary team may include:

• Paediatrician or developmental specialist.
• Paediatric neurologist.
• Orthopaedic surgeon.
• Physiatrist.
• Physiotherapist.
• Occupational therapist.
• Orthotist.
• Speech and language therapist.
• Nutrition team.
• Rehabilitation and wheelchair/seating specialists.

• Treating spasticity without assessing fixed deformity.
• Assuming every tight muscle requires surgical lengthening.
• Ignoring muscle weakness when treating contracture.
• Correcting one joint without assessing the entire limb.
• Failure to recognise torsional deformity and lever-arm dysfunction.
• Over-lengthening the Achilles/gastrocsoleus complex and producing weakness.
• Failing to perform hip surveillance in high-risk children.
• Waiting until the hip is painfully dislocated before referral.
• Using radiographic correction as the only measure of surgical success.

• Cerebral palsy results from a non-progressive lesion of the developing brain, but musculoskeletal deformities may progress during growth.
• Spastic CP is the commonest motor type.
• GMFCS classifies gross motor function into five levels.
• Children at higher GMFCS levels have a greater risk of progressive hip displacement.
• Hip displacement in CP is generally acquired and progressive rather than congenital.
• Reimers migration percentage is used to quantify lateral migration of the femoral head.
• A migration percentage above approximately 30% is commonly regarded as abnormal and warrants closer surveillance.
• Varus derotation osteotomy is an important reconstructive procedure for progressive hip displacement.
• Silfverskiöld test differentiates isolated gastrocnemius tightness from combined gastrocsoleus contracture.
• Duncan-Ely test assesses rectus femoris spasticity/tightness.
• Popliteal angle is used to assess hamstring length.
• Excessive femoral anteversion and external tibial torsion contribute to lever-arm dysfunction.
• Excessive plantar-flexor lengthening can contribute to crouch gait.
• Crouch gait is characterised by excessive hip and knee flexion during stance.
• Rectus femoris overactivity may contribute to stiff-knee gait.
• Botulinum toxin is most useful for selected dynamic focal spasticity rather than fixed bony deformity.
• SEMLS = Single-Event Multilevel Surgery.
• SEMLS aims to correct multiple clinically important gait abnormalities during a single operative episode.
• In non-ambulatory patients, goals commonly include comfort, stable sitting, hip stability, hygiene and ease of care rather than restoration of walking.

1. Classify function first: GMFCS level guides prognosis, surveillance and treatment goals.
2. Distinguish dynamic from fixed deformity: spasticity and structural contracture require different treatment.
3. Monitor the hips: progressive hip displacement is one of the most important preventable orthopaedic complications.
4. Analyse the entire limb: deformity at the hip, knee, ankle, foot and rotational level interacts during gait.
5. Preserve muscle strength: unnecessary or excessive tendon lengthening can worsen function.
6. Correct lever-arm dysfunction: femoral and tibial torsional deformities may require osteotomy.
7. Use multilevel planning: ambulatory children frequently benefit from coordinated treatment of several abnormalities rather than isolated procedures.
8. Individualise goals: gait efficiency may be the priority in an ambulatory child, whereas comfort, sitting and hygiene may be more important in a non-ambulatory child.
9. Combine surgery with rehabilitation: orthopaedic reconstruction is only one component of multidisciplinary cerebral palsy care.

The orthopaedic treatment of cerebral palsy is not aimed at treating the brain lesion. It aims to prevent or correct the progressive musculoskeletal consequences of abnormal tone, weakness and growth while maximising the patient's function, comfort and quality of life.