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Presentation of cerebral palsy

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ChairpersonDr. R. S. Jatti Presenter Dr. Srinath Gupta Cerebral Palsy
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Page 1: Presentation of cerebral palsy

ChairpersonDr. R. S. Jatti Presenter Dr. Srinath

Gupta

Cerebral Palsy

Page 2: Presentation of cerebral palsy

Brain Development Brain grossly differentiates into cerebrum

and cerebellum during 1st Trimester of embryonic life

Neurons begin to develop in 2nd trimester By end of 2nd trimester all neurons are

formed and any damage occurring now is irreversible

Synaptic connections occur in 3rd trimester

Page 3: Presentation of cerebral palsy

First described in 1862, by William John Little, an orthopedic surgeon who observed that children with tone and developmental abnormalities often had prolonged labor, prematurity or breech delivery

Cerebral Palsy was known as Little’s Disease for decades.

The term cerebral Palsy originated with William Osler and Sigmund Freud

Static Encephalopathy has been used interchangeably with cerebral palsy

Trivia

Page 4: Presentation of cerebral palsy

Overview Definition Incidence Etiology Classification Management Lower Limb Deformities

Page 5: Presentation of cerebral palsy

Definition Static, non progressive disorder of CNS

secondary to an insult to immature brain, resulting in varying degrees of motor milestone delay and dysfunction

CP is a disorder of tone, posture or movement

It results in paralysis, weakness, in coordination or abnormal movement

Page 6: Presentation of cerebral palsy

Incidence 2.4-2.7 for every 1000 live births

Page 7: Presentation of cerebral palsy

EtiologyPrenatal:

◦Infection: TORCH Complex, HIV◦Cerebral malformation◦Obstetrical complication: pre-eclampsia,

eclampsia, abruptio placentae, placenta previa, placental infarction

◦Maternal diseases◦Abuse of drugs

Page 8: Presentation of cerebral palsy

Contd…Perinatal:

◦Prematurity◦Low birth weight◦Complicated delivery◦Asphyxia◦Cerebral trauma◦Hyperbilirubinemia◦Blood incompatibilities◦Infections: Herpes simplex, meningitis◦Severe hypoglycemia

Page 9: Presentation of cerebral palsy

Contd…Post natal :

◦ Infections : Meningitis, encephalitis◦ Head injury◦ Cerebral anoxia◦ Aspiration◦ Asphyxia◦ Seizures◦ Near drowning◦ Cardiac arrest◦ Cerebrovascular accidents◦ Sickle cell anaemia◦ Vascular malformations

Page 10: Presentation of cerebral palsy

Classification Because of the wide variability in presentation and

types of cerebral palsy, there is no universally accepted classification scheme.

Page 11: Presentation of cerebral palsy

Monoplegia Hemiplegia Paraplegia Diplegia Quadriplegia Double Hemiplegia Total body

Classification based on Geographical Distribution

Page 12: Presentation of cerebral palsy

Physiological classification Spastic Athetoid Choreiform Rigid Ataxic Hypotonic Mixed

Page 13: Presentation of cerebral palsy

Spastic:◦ Most common type◦ Associated with injury to pyramidal tracts in immature brain

Athetoid:◦ Associated with injury to extrapyramidal tracts◦ Dyskinetic purposeless movements◦ Dystonia or hypotonia can occur with athetoid cerebral palsy

Choreiform:◦ Continual purposeless movements of wrists,fingers,toes and

ankles

Contd…

Page 14: Presentation of cerebral palsy

Rigid:◦ Most hypertonic form◦ Cogwheel or leadpipe rigidity

Ataxic:◦ Very rare◦ Injury to developing cerebellum◦ Disturbance of coordinated movement viz. walking◦ Characterized by weakness, in-coordination, a wide

based gait, and trouble with fine and rapid movements. 

Hypotonic:◦ Passing stage in spastic or ataxic cerebral palsy

Mixed:◦ Signs of pyramidal and extrapyramidal deficits

Contd…

Page 15: Presentation of cerebral palsy

Spastic Diplegia•Bilateral spasticity of legs•1st noticed when infant begins to crawl-tends to drag the legs behind more ( commando crawl)•Severe spasticity –application of diaper is difficult due to excess adduction of hips•Brisk reflexes, ankle clonus•Scissoring posture of lower extremity when suspended by axilla

•Walking tiptoes, disuse atropy ,impaired growth of lower extremity•Intellectual development normal•Minimal seizures •CT/MRI-periventricular leukomalacia of white matter mainly lower limb fibres•All spastic types characterized by toe walking, a crouched gait, and flexed knee, scissoring

Page 16: Presentation of cerebral palsy

Spastic Hemiplegia•Arms often more involved than leg-difficulty in hand manipulation is obvious by 1 yr•Delayed walking -18-24 months•Equinovarus deformity of foot, walks on tip toes because of increased tone•Affected upper limb has dystonic posture when child runs

•Deep tendon reflexes increased, ankle clonus, Babinski sign +•1/3rd have seizure disorder•25% have MR•CT/MRI- atrophic cerebral hemisphere with dilated lateral ventricle contralateral to the affected side

Page 17: Presentation of cerebral palsy

Spastic Quadreplegia•Most severe form ,most common•All extremities severely impaired•High association with MR and seizures•Flexion Contractures of knees and elbows

Page 18: Presentation of cerebral palsy

After age 1yr –athetoid movements become evident

Speech is affected (slurred, voice modulation impaired) due to involvement of oropharyngeal muscles

Upper motor neuron signs –not present

Seizure uncommon Intellect –preserved Characterized by an exaggerated step,

hip and knee hyperextension, a backwards lean, and shoulder girdle and trunk extension.

Athetoid Cerebral palsy

Page 19: Presentation of cerebral palsy

I Has nearly normal gross motor function II Walks independently, but has limitations with

running and jumping III Uses assistive devices to walk and wheelchair

for long distances IV Has ability to stand for transfers, but minimal

walking ability; depends on wheelchair for mobility

V Lacks head control, can’t sit independently, is dependent for all aspects of care

Gross Motor Function Classification System

Page 20: Presentation of cerebral palsy

Associated Problems Mental Retardation Communication Disorders Behavioral disorder Seizures Vision Disorders Hearing loss Somatosensation (skin sensation, body awareness)

Temperature instability Nutrition Drooling Dentition problems Neurogenic bladder Neurogenic bowel Gastroesophageal reflux Dysphagia Autonomic dysfunction

Page 21: Presentation of cerebral palsy

Gait in cerebral palsy◦Idiopathic toe walking◦Spastic knee gait◦Crouch gait

Gait

Page 22: Presentation of cerebral palsy

Determine grades of muscle strength and selective control.

Evaluate muscle tone and determine type. Evaluate degree of deformity / contracture at each joint. Assess linear, angular and torsional deformities of

spine, long bones, hands and feet. Appraise balance, equilibrium and standing / walking

posture.

Clinical AssessmentGoals of Physical Examination

Page 23: Presentation of cerebral palsy

History Examination X-ray skull-intracranial calcification EEG CT/MRI Test of hearing ,vision IQ test

Diagnosis

Page 24: Presentation of cerebral palsy

Achievable goals should be set The child with CP becomes the adult with CP

Goals based on needs of adults Communication : verbal / nonverbal Mobility Walking Activity of daily living (ADL) feeding, dressing, toileting, bathing Turn focus of parents from the disease to the

goal-oriented approach

Goals of Management (Treatment)

Page 25: Presentation of cerebral palsy

Control of spasticityPhysical therapyOrthoticsOrthopedic surgery

Types of Management (Treatment)

Page 26: Presentation of cerebral palsy

Spasticity is present in most patients with CP (65 % ) When it is reduced patients may : - perform integrated muscle movement - develop muscle strength - function at a higher level Approaches :

• Selective dorsal rhizotomy• Intrathecal baclofen• Botulinum-A toxin

CONTROL OF SPASTICITY

Page 27: Presentation of cerebral palsy

Other oral medicines used in Cerebral Palsy:◦ Dantrolene◦ Flexeril◦ Antiepileptic drugs such as Phenytoin, Sodium Valproate,

Carbamazepine, etc.

Page 28: Presentation of cerebral palsy

Conventional PT :◦ Works on muscles, tendons, and ligaments

Active exercises Passive ROM exercises Passive stretching Bracing

PHYSICAL THERAPY

Page 29: Presentation of cerebral palsy

Involve parents as much as possible (even if they resist)

Do not raise false hopeswhich could increase frustration

Contd…

Page 30: Presentation of cerebral palsy

ORTHOTICSCasting..Short leg casts are applied with extended toe plates, careful

molding of the heel and metatarsal head control.For a period of time varies but usually a minimum of 6 weeks.

and is followed by the use of orthoses.There is a limited role for casting in patients with cerebral palsy.

Orthoses..Can be helpful in improving gait in ambulatory patient with

cerebral palsy.Ankle-foot orthoses are most commonly prescribed to assist the

child with positioning of the ankle and foot during gait.

Page 31: Presentation of cerebral palsy

Ankle Foot Orthoses (AFO)

Page 32: Presentation of cerebral palsy

m

Orthoses

Page 33: Presentation of cerebral palsy

Primary deformity : needs treatment

Compensatory deformity : can improve without intervention

Surgery Prevent structural changes - usually early

Improve function - usually later

ORTHOPEDIC PROCEDURESDistinguish between

Page 34: Presentation of cerebral palsy

Type : spastic Extent : hemiplegics / diplegics : good results quadriplegics : minimal improvement Age : 3- 12 years IQ : good Good upper limb function : for walking Underlying muscle power : not weak Walker / non-walker : surgery hardly changes state but improves gait

Prerequisites for effective surgery

Page 35: Presentation of cerebral palsy

For structural changes : Early e.g. Hip subluxation , usually <5 years To improve function ( gait ) : defer until walking ( independently / with aids ) until gait pattern develops and can be assessed walking : 18 – 21 months in hemiplegia 3 – 4 years in spastic diplegia Optimum time of lower extremity surgery 5 – 7 years: can analyze and observe gait pattern

Timing For Orthopaedic Surgery

Page 36: Presentation of cerebral palsy

Timing For Orthopaedic Surgery

Surgery should not be unduly staged one by one ( with each birthday )

?ETA ? Hams ? Psoas ? Rectus Femoris

Equinus Crouch Flexion Stiff Knee Ok

Page 37: Presentation of cerebral palsy

Hip◦ Flexion contracture◦ Increased hip addduction/ scissoring◦ Subluxating or dislocating hip

Rotational deformities of femur and tibia Knee Foot

◦ Equinus◦ Equinovarus◦ Pes valgus◦ Ankle valgus◦ Hallux valgus◦ Dorsal Bunion

Lower limb involvement

Page 38: Presentation of cerebral palsy

Adduction and flexion deformity Hip at risk Hip subluxation Hip dislocation

Hip Problems

Page 39: Presentation of cerebral palsy

Hip flexion contractures are found most commonly in patients with spastic diplegia and spastic quadriplegia.

Flexion contracture is due to increased tone in the hip flexors (primarily the iliopsoas) and relative weakness of the hip extensors (such as the gluteal muscles)

The contracture is identified during the physical examination by performing the Thomas and Staheli maneuvers.

Flexion Deformities in Hip

Page 40: Presentation of cerebral palsy

Thomas test

Staheli test

Page 41: Presentation of cerebral palsy

Clinical AssessmentHip Flexors

Ely / Rectus Femoris Test

Page 42: Presentation of cerebral palsy

Flexion internal rotation deformity should be differentiated from True Adduction deformity.

Increased femoral anteversion when combined with crouch at the knee can produce the appearance of scissoring which termed as pseudo adduction

Adductor surgery will be ineffective in improving the child’s ability to walk when the narrow base of gait is secondary to pseudo adduction.

Page 43: Presentation of cerebral palsy

Single-stage multilevel procedures are preferable to staged single-level procedures because hospitalization, immobilization, and rehabilitation time and the number of anesthetic exposures are decreased

Hip flexion contractures from 15 to 30 degrees usually are treated with psoas lengthening

Contractures of more than 30 degrees may require more extensive releases of the rectus femoris, sartorius, and tensor fasciae latae and the anterior fibers of the gluteus minimus and medius, in addition to the iliopsoas

Treatment

Page 44: Presentation of cerebral palsy

Iliopsoas recession (Skaggs et al technique)

Contd…

Page 45: Presentation of cerebral palsy

Iliopsoas release at the Lesser trochanter(Miller technique)

Page 46: Presentation of cerebral palsy

Iliopsoas tenotomy / lengthening / recession

Tenotomy : Should not be done in ambulatory patients

Recession : Doesn’t cause excessive hip flexion weakness

Lengthening (z plasty) : best / easy /satisfactory in ambulating patients no risk of too much weakening of flexion power

Contd…

Page 47: Presentation of cerebral palsy

Most common deformity Spasticity in the adductor muscles in cerebral palsy results

in a narrow base of gait and scissoring, hip subluxation, and, in severely affected children, difficulty with perineal hygiene

Adduction deformities in Hip

Page 48: Presentation of cerebral palsy

Adductor tenotomy and release◦ Resection of tendon of adductor longus and anterior half of

addductor brevis and gracilis ,if required◦ Avoid neurectomy of ant. branch of obturator nerve

Operative treatment:

Page 49: Presentation of cerebral palsy

Deformities of the hip in patients with cerebral palsy range from mild painless subluxation to complete dislocation with joint destruction, pain, and impaired mobility

In most patients, the hip is normal at birth, and radiographic changes typically become apparent between 2 and 4 years of age.

Subluxation and dislocation

Page 50: Presentation of cerebral palsy

Hip subluxation in patients with cerebral palsy can be difficult to detect clinically

Routine clinical and radiographic examinations should be done every 6 months

A practical radiographic method for quantifying the amount of hip subluxation present, which was described by Reimers as the “migration percentage.”

Page 51: Presentation of cerebral palsy

Hip subluxation ( partially out)Hilgenreiner line

Contd…

Dislocated Subluxated50 %

Reimer’s migration index

Page 52: Presentation of cerebral palsy

Hip subluxation ( partially out )( > 30 % uncoverage / broken Shenton’s line )

Contd…

Page 53: Presentation of cerebral palsy

Hip at risk

Because early intervention can be very effective in preventing or delaying the development of dislocation, considerable work has been done to identify hips at risk

Page 54: Presentation of cerebral palsy

Hip at Risk Hip subluxation

Contd…

At 2.5 years At 7 years

Page 55: Presentation of cerebral palsy

Varus Derotational Osteotomy, usually combined with soft-tissue releases, is indicated for patients with excessive anteversion and valgus deformity of the proximal femur and a hip that is either subluxated or dislocated

Operative Treatment

Page 56: Presentation of cerebral palsy
Page 57: Presentation of cerebral palsy

Combined One-Stage Correction of Spastic Dislocated Hip (San Diego Procedure) ◦ medial approach (soft-tissue release) ◦ anterior approach (open reduction)◦ lateral approach (femoral osteotomy) ◦ anterior approach (pericapsular pelvic osteotomy)

Operative treatment

Page 58: Presentation of cerebral palsy

Proximal Femoral Resection

Painful dislocated > 1 year

Surgical resection

Page 59: Presentation of cerebral palsy

Hip Arthrodesis The ideal candidate is a patient with unilateral disease and no spinal involvement. Hip arthrodesis may be preferable in ambulatory patients because it allows weight bearing, in contrast to proximal femoral resections.

Contd…

Page 60: Presentation of cerebral palsy

Deformities of the knee rarely occur in isolation

The hip and the knee are tightly coupled because of the muscles that cross both joints, the “two-joint muscles.”

KNEE

Page 61: Presentation of cerebral palsy

Flexion Deformity Recurvatum of the Knee Knee Valgus Patella Alta

Deformities in knee

Page 62: Presentation of cerebral palsy

Most common knee deformity in patients with cerebral palsy and frequently occurs in ambulatory children

Crouching gait.

Flexion Deformity

Page 63: Presentation of cerebral palsy

Straight leg raising◦ Angle< 70 … Indication

The Hamstring Test◦ Holt’s method◦ Popliteal Angle< 135 - Indication

Clinical AssessmentKnee Flexion

Page 64: Presentation of cerebral palsy

Fractional Lengthening of Hamstring Tendons

Operative management

Page 65: Presentation of cerebral palsy

Distal Transfer of Rectus Femoris

Page 66: Presentation of cerebral palsy

Combined Hamstring Lengthening and Quadriceps Shortening along with posterior capsule release

Page 67: Presentation of cerebral palsy

Hip flexion Deformity increases after

hamstring release

Better to transfer hamstring insertion to keep hip extended

Effect of Knee Surgery on The Hip

Page 68: Presentation of cerebral palsy

Caused by Quadriceps spasticity or long standing Knee FFD.

Can lead to repeated to micro trauma to patellar tendon and quadriceps tendon and stress fractures of patella and tibial tubercle.

Usually painless, so intervention is not required.

Correction of FFD of knee with hamstring lengthening causes improvement.

Patella alta

Page 69: Presentation of cerebral palsy

DEFORMITIES◦ Equinus Deformity◦ Varus or Valgus Deformity

Equinovarus Deformity Equinovalgus Deformity

◦ Calcaneus Deformity◦ Cavus Deformity◦ Forefoot Adduction Deformity◦ Hallux Valgus Deformity◦ Claw Toes

FOOT

Page 70: Presentation of cerebral palsy

Most common foot deformity in patients with cerebral palsy

It is an increased plantar flexion due to a plantar flexion contracture or dynamic plantar flexion due to over activity of the gastrocsoleus during gait

Equinus deformity

Page 71: Presentation of cerebral palsy

Toe-walking patients must be considered as two different groups:◦ equinus patients◦ as a consequence of crouch at the hip and knee with

natural ankle. Cerebral palsy must be differentiated from:

Idiopathic toe walking as a congenital short Achilles tendon

Muscular dystrophy (as Duchenne’s)produces toe walking.

Page 72: Presentation of cerebral palsy

Equinus.. Clinical examination..

Inability to fully dorsiflex the ankle

The Silverskiold test:If the ankle can be passively dorsiflexed with the knee bent to 90 degree but cannot be dorsiflexed with the knee extended it is believed that the gastrocnemius is tight, but the soleus is not contracted

This test is used to determine which type of surgical lengthening to perform

Page 73: Presentation of cerebral palsy

The Silfverskiold test

Page 74: Presentation of cerebral palsy

Dynamic : Treat by : Bracing Spasticity reduction Surgery Fixed : Treat by : Serial casting Surgery

Treatment

Page 75: Presentation of cerebral palsy

Open Lengthening of the Achilles Tendon

Surgical treatment

Page 76: Presentation of cerebral palsy

Z-Plasty Lengthening of the Achilles Tendon

Page 77: Presentation of cerebral palsy

Percutaneous Lengthening of the Achilles Tendon

Page 78: Presentation of cerebral palsy

Lengthening of the Gastrocnemius-Soleus Muscle

Vulpius technique.. Strayer procedure

Page 79: Presentation of cerebral palsy

Baker technique(tongue-in-groove)

Page 80: Presentation of cerebral palsy

Diplegic patients typically have internally rotated and adducted hips, flexed knees, and external rotation deformity of the tibia. This combination of deformities causes the foot to assume a valgus position.

In hemiplegic patients, the internally rotated thigh with the knee coming to full extension in stance phase causes the foot to internally rotate and produce a varus deformity

Varus or Valgus Deformity

Page 81: Presentation of cerebral palsy

Muscle imbalance in which the invertors of the foot over power the evertors, most commonly Tibialis post.

Gastrocnemius contributing equinus

Surgery is indicated to1. Improve foot contact.2. Relieve pain.3. Relieve skin changes

Equinovarus Deformity

Page 82: Presentation of cerebral palsy

Contd…The confusion test:

The patient flexes the hip against resistance If supination of the forefoot is seen, then

anterior tibialis is contributing to equinovarus deformity .When dorsiflexion is seen without supination, the deformity is less likely to respond to surgery on the anterior tibialis

Page 83: Presentation of cerebral palsy

It also is important to determine whether or not the deformity is flexible and correctable or rigid because patients with flexible deformities are more likely to be successfully treated nonoperatively with orthotics and shoe modifications and operatively with soft-tissue procedures such as tendon lengthenings, releases, or transfers (usually of the abnormally active muscle)

Patients with rigid varus deformities generally require bone procedures, such as calcaneal osteotomy.

Contd…

Page 84: Presentation of cerebral palsy

Lengthening of the Posterior Tibial Tendon◦ Z-Plasty Lengthening of the Posterior Tibial Tendon◦ Step-Cut Lengthening of the Posterior Tibial Tendon◦ Intramuscular lengthening of the Posterior Tibial Tendon

Surgical treatment

Page 85: Presentation of cerebral palsy

Split Tendon Transfers◦ Split posterior tibial

tendon transferIt is one of the most

common procedures for equinovarus deformity treatment.

The posterior one-half of the posterior tibialis tendon is rerouted posterior to tibia and woven into the peroneus brevis

tendon.

Contd…

Page 86: Presentation of cerebral palsy

Kaufer split transfer of tibialis posterior tendon

Page 87: Presentation of cerebral palsy

Kaufer split transfer of tibialis posterior tendon

Page 88: Presentation of cerebral palsy

◦ Split anterior tibial tendon transfer

The lateral one-half of anterior tibialis is detached from its insertion.

Passed beneath the extensor retinaculum.Inserted through a bone tunnel into the cuboid.Foot is positioned in 5-10 deg. of dorsiflexion.Known as the Rancho procedure when done in combination

with posterior tibialis lengthening.

Contd…

Page 89: Presentation of cerebral palsy

Split transfer of tibialis anterior tendon

Page 90: Presentation of cerebral palsy

Heel varus will respond to calcaneal osteotomy.

If the deformity is severe, and with rigid component of mid foot supination… Triple arthrodesis should be performed.

Even with bony procedures, muscle imbalance must be corrected.

Bony surgery in Equinovarus

Page 91: Presentation of cerebral palsy

Dwyer closing wedge osteotomy of calcaneus for varus heel

Page 92: Presentation of cerebral palsy

Pes valgus Occurs in up to 25% of patients with cerebral palsy.

and most common in older diplegic or quadriplegic patients.

Can be caused by spastic peroneal muscles, weakness of the p.tibialis and a tight gastrocsoleus.

Radiographs should be obtained in standing position for the foot and ankle.

Conservative treatment should vigorously pursued.. shoe inserts and orthoses may be adequate to relive pain and avoiding surgery.

Page 93: Presentation of cerebral palsy
Page 94: Presentation of cerebral palsy

Surgical treatment of Pes valgus

Bony surgery is the only predictable alternative for full and lasting correction.

Surgical options are…I. The Grice extra- articular arthrodesis.II. Lateral column (calcaneal neck) lengthening.III. Calcaneal osteotomy.IV. Triple arthrodesis.

Page 95: Presentation of cerebral palsy

Grice extra- articular arthrodesis Modifications to the original procedure:

Fibular graft was changed to iliac crest graft. Using internal fixation to keep the position of the subtalar joint in

combination with cancellous iliac crest graft.

Page 96: Presentation of cerebral palsy

Calcaneal osteotomy

Advantage: preserve joint motion of sub talar joint.

Results have been very good.

Contraindications: severe rigid valgus deformity.

Page 97: Presentation of cerebral palsy

Triple Arthrodesis Treatment of choice for rigid symptomatic Pes valgus in adolescent

with cerebral palsy. Resecting the subtalar, calcaneocuboid, talonavicular joints.

Indications:1. Pain2. Skin ulceration over the talar head.3. Deformity interfering with ambulation in child with deformity not

amenable to osteotomy. Satisfactory outcomes are found when deformity is well corrected.

Degenerative changes have been documented in the ankle joint at an average of 18yrs.following arthrodesis in 43% of the pediatric population.

Page 98: Presentation of cerebral palsy

Triple arthrodesis for Pes valgus treatment

Page 99: Presentation of cerebral palsy

Dorsal bunion It is a rare deformity. The first metatarsal head is elevated, but

the great toe is plantar flexed.

Surgical rebalance depends on…Transfer of the flexor tendon to the extensor.Or flexor tenotomy.Or by transferring of the flexor hallucis brevis

to the metatarsal neckOr by all that in combination with closing

wedge plantar flexion osteotomy of first metatarsal.

Page 100: Presentation of cerebral palsy

Hallux valgus Develops in cerebral palsy patients in response to a Equino valgus deformity of the

hind foot. There is a progressive eversion and abduction of foot because of peroneus longus

is spastic. The toe is pushed laterally as weight is borne by the everted foot. The big toe comes to lie beneath the second toe, and the first metatarsal head

becomes uncovered and painful bunion develops.

When this deformity is mild, surgical treatment of Pes valgus will halt the progression of toe deformity.

Bleck& Goldner described soft tissue realignment including:Release of the adductor hallucis t. and lateral capsulotomy of the first metatarsophalangeal

joint. combined with first metatarsal and proximal phalangeal osteotomy.

McKeveer technique: First metatarsophalangeal fusion. That led to better results with less recurrence than soft tissue realignment.

Preferred position for fusion is 15-25 deg. Of dorsiflexion and slight valgus.

Page 101: Presentation of cerebral palsy

Hallux valgus in 14 yrs. Old girl with cerebral palsy.Treated with metatarsophalangeal fusion.

Page 102: Presentation of cerebral palsy

Intoeing Usually caused by femoral ante-version Internal tibial torsion adds to Intoeing Not related to spasticity of internal

rotators

If severe : Derotation osteotomy Delay to late childhood if

possible

Derotation osteotomy of femur might cause tightening of medial hamstrings

( might need lengthening )

Page 103: Presentation of cerebral palsy

In-toeing

Page 104: Presentation of cerebral palsy

Why Does Anteversion Cause In-toeing ?

Anteversion rotates Greater Trochanter posteriorly

On stance phase need Abductor power Abductor power optimized when Greater

Trochanter is lateral not posterior Internal rotation in stance phase brings

Greater Trochanter laterally

Page 105: Presentation of cerebral palsy

In-toeingIndication for derotation osteotomy

Severe femoral anteversion, with loss of all external rotation.

Dynamic in-toeing causing gait abnormalities. Dynamic in-toeing causing secondary foot

deformity. Usually not before 8-10 years.

Page 106: Presentation of cerebral palsy

THANK YOU…!!


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