Chairperson Dr. R. S. Jatti
Presenter Dr. Srinath Gupta
Brain grossly differentiates into cerebrum
and cerebellum during 1st Trimester of
Neurons begin to develop in 2nd trimester
By end of 2nd trimester all neurons are
formed and any damage occurring now is
Synaptic connections occur in 3rd
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
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
Static, non progressive disorder of CNS secondary
to an insult to immature brain, resulting in
varying degrees of motor milestone delay and
CP is a disorder of tone, posture or movement
It results in paralysis, weakness, in coordination
or abnormal movement
◦ Most common type
◦ Associated with injury to pyramidal tracts in immature
◦ Associated with injury to extrapyramidal tracts
◦ Dyskinetic purposeless movements
◦ Dystonia or hypotonia can occur with athetoid cerebral
◦ Continual purposeless movements of wrists,fingers,toes
◦ Most hypertonic form
◦ Cogwheel or leadpipe rigidity
◦ Very rare
◦ Injury to developing cerebellum
◦ Disturbance of coordinated movement viz.
◦ Characterized by weakness, in-coordination, a
wide based gait, and trouble with fine and rapid
◦ Passing stage in spastic or ataxic cerebral palsy
◦ Signs of pyramidal and extrapyramidal deficits
•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
•Walking tiptoes, disuse atropy ,impaired
growth of lower extremity
•Intellectual development normal
•CT/MRI-periventricular leukomalacia of
white matter mainly lower limb fibres
•All spastic types characterized by toe
walking, a crouched gait, and flexed
•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
•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
•Most severe form ,most
•All extremities severely
•High association with MR
•Flexion Contractures of
knees and elbows
After age 1yr –athetoid movements
Speech is affected (slurred, voice
modulation impaired) due to
involvement of oropharyngeal muscles
Upper motor neuron signs –not
Characterized by an exaggerated step,
hip and knee hyperextension, a
backwards lean, and shoulder girdle
and trunk extension.
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
V Lacks head control, can’t sit independently, is
dependent for all aspects of care
Gait in cerebral palsy
◦ Idiopathic toe walking
◦ Spastic knee gait
◦ Crouch gait
Determine grades of muscle strength and selective
Evaluate muscle tone and determine type.
Evaluate degree of deformity / contracture at each
Assess linear, angular and torsional deformities of
spine, long bones, hands and feet.
Appraise balance, equilibrium and standing / walking
X-ray skull-intracranial calcification
Test of hearing ,vision
Achievable goals should be set
The child with CP becomes the adult with CP
Goals based on needs of adults
Communication : verbal / nonverbal
Activity of daily living (ADL)
feeding, dressing, toileting, bathing
Turn focus of parents from the disease to the
Control of spasticity
Spasticity is present in most patients with CP (65 % )
When it is reduced patients may :
- perform integrated muscle
- develop muscle strength
- function at a higher level
• Selective dorsal rhizotomy
• Intrathecal baclofen
• Botulinum-A toxin
Other oral medicines used in Cerebral Palsy:
◦ Antiepileptic drugs such as Phenytoin, Sodium Valproate,
Conventional PT :
◦ Works on muscles, tendons, and ligaments
Passive ROM exercises
Involve parents as much as possible
(even if they resist)
Do not raise false hopes
which could increase frustration
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
Can be helpful in improving gait in ambulatory patient with
Ankle-foot orthoses are most commonly prescribed to assist
the child with positioning of the ankle and foot during gait.
Primary deformity : needs treatment
Compensatory deformity : can improve without intervention
Prevent structural changes - usually early
Improve function - usually later
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
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
Surgery should not be unduly staged one by
( with each birthday )
?ETA ? Hams ? Psoas ? Rectus Femoris
Equinus Crouch Flexion Stiff Knee Ok
◦ Flexion contracture
◦ Increased hip addduction/ scissoring
◦ Subluxating or dislocating hip
Rotational deformities of femur and tibia
◦ Pes valgus
◦ Ankle valgus
◦ Hallux valgus
◦ Dorsal Bunion
Adduction and flexion deformity
Hip at risk
Hip flexion contractures are found most commonly
in patients with spastic diplegia and spastic
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
The contracture is identified during the physical
examination by performing the Thomas and
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.
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
Iliopsoas recession (Skaggs et al technique)
Iliopsoas release at the Lesser trochanter(Miller
Iliopsoas tenotomy / lengthening /
Tenotomy : Should not be done in
Recession : Doesn’t cause excessive hip
Lengthening (z plasty) : best / easy
/satisfactory in ambulating patients no
risk of too much weakening of flexion
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
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
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.
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.”
Hip subluxation ( partially out)
Hip subluxation ( partially out )
( > 30 % uncoverage / broken Shenton’s line )
Because early intervention can be very effective in
preventing or delaying the development of dislocation,
considerable work has been done to identify hips at
Hip at Risk Hip subluxation
At 2.5 years At 7 years
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
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)
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
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
Recurvatum of the Knee
Most common knee deformity in patients with
cerebral palsy and frequently occurs in ambulatory
Straight leg raising
◦ Angle< 70 … Indication
The Hamstring Test
◦ Holt’s method
◦ Popliteal Angle< 135 - Indication
Combined Hamstring Lengthening and
Quadriceps Shortening along with posterior
Hip flexion Deformity
Better to transfer
to keep hip extended
Caused by Quadriceps spasticity or long standing
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.
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
Toe-walking patients must be considered as two
◦ equinus patients
◦ as a consequence of crouch at the hip and knee with
Cerebral palsy must be differentiated from:
Idiopathic toe walking as a congenital short Achilles
Muscular dystrophy (as Duchenne’s)produces toe
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
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
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
Muscle imbalance in which
the invertors of the foot over
power the evertors, most
commonly Tibialis post.
Surgery is indicated to
1. Improve foot contact.
2. Relieve pain.
3. Relieve skin changes
The confusion test:
The patient flexes the hip against
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
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.
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
◦ Split posterior tibial
It is one of the most common
procedures for equinovarus
The posterior one-half of the
posterior tibialis tendon is
rerouted posterior to tibia and
woven into the peroneus brevis
◦ Split anterior tibial tendon transfer
The lateral one-half of anterior tibialis is detached from its
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.
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.
Occurs in up to 25% of patients with cerebral palsy.
and most common in older diplegic or quadriplegic
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.
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.
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.
joint motion of sub
Results have been very
severe rigid valgus
Treatment of choice for rigid symptomatic Pes valgus in adolescent
with cerebral palsy.
Resecting the subtalar, calcaneocuboid, talonavicular joints.
2. 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
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 neck
Or by all that in combination with closing
wedge plantar flexion osteotomy of first
Develops in cerebral palsy patients in response to a Equino valgus deformity of the
There is a progressive eversion and abduction of foot because of peroneus longus is
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.
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.
Hallux valgus in 14 yrs. Old girl with cerebral palsy.
Treated with metatarsophalangeal fusion.
Usually caused by femoral ante-
Internal tibial torsion adds to Intoeing
Not related to spasticity of internal
If severe : Derotation osteotomy
Delay to late childhood if
Derotation osteotomy of femur might
cause tightening of medial hamstrings
( might need lengthening )
Anteversion rotates Greater Trochanter
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
Severe femoral anteversion, with loss of all
Dynamic in-toeing causing gait abnormalities.
Dynamic in-toeing causing secondary foot
Usually not before 8-10 years.
Static, non progressive disorder of CNS secondary to an insult to immature brain, resulting in varying degrees of motor milestone delay and dysfunction
----- Meeting Notes (8/7/15 13:57) -----
Spastic – Pyramidal tract (Corticospinal and Cortico bulbar) Rest – Extra pyramidal tracts (reticulospinal, rubrospinal, tectospinal, vestibulospinal)
Spastic knee gait - limited knee flexion in swing phase due to rectus femoris firing out of phase (seen on EMG) Crouch gait – Combination of hip flexion, knee flexion, and ankle equinus
Electroencephalography (EEG) is the recording of electrical activity along the scalp. EEG measures voltage fluctuations resulting from ionic current flows within the neurons of the brain
Rhizotomy - Cut 30 – 50 % of abnormal dorsal rootlets L2 - S1 Followed by intensive physiotherapy. Results are encouraging Best for :spastic diplegia 4-8 yrs no previous surgery no contracture no extra pyramidal signs. Intrathecal - GABA agonist- inhibits release of excitatory neurotransmitter at level of spinal cord Botulinum - Inhibits exocytosis of Acetylcholine
There is no evidence that any type of physical therapy can have a beneficial lasting effect on motor function beyond early to middle childhood (age 4-8 years) Thomas S. Renshaw ( Lovell & Winter’s Pediatric Orthopaedics) So, spend time in improving developmental and cognitive skills.
Hip Flexors- Iliopsoa (primary) Secondary – Sartorius, Rectus femoris, Adductor longus. Extensors – Gluteus maximus ( More powerful with knee flexed) Hamstrings – Semimemb, SemiT, Biceps Femoris (with knee extended)
Skaggs et al –DONE IF HIP INTERNALLY ROTATES DURING WALKING AND EXTERNAL ROTATION IS PRESENT ONLY IF HIP IS FLEXED TO 90 DEGREES. Patient in supine position with a roll under the buttocks. 5 cm bikini incision. Identify interval betwn tfl and sartorius. See direct head of rectus femoris (aiis origin) Palpate pelvis brim. Identify iliopsoas tendon jus medial and inferior to rectus femoris. Pull iliopsoas muscle medially to expose psoas tendon. Internally rotate and externally rotate to see the tightening and loosening of the tendon and release tendinous portion.
MILLER TECH – Better for nonambulatory ptns. Because it leads to excessive hip flexion weakness(so not done in ambulatory patients) Commonly done with adductor release or varus derotation osteotomy. 1 To 3 cm transverse incision distal to inguinal crease. IF ADDUCTOR RELEASE TO BE DONE – incise adductor longus fascia. And transect adductor longus with cautery. Myotomy of gracilis. Resect adductor brevis till 45 degrees abduction is achieved. Identify iliopsoas bursa and open it. Retract tendon medially. In non ambulatory patient, release completely. In ambulatory, release as much proximally as possible. This preserves iliacus muscle attachment to the tendon.
Longus- ORIGIN – Flat tendon from front of body of pubis in the angle between pubic crest and symphysis. Brevis – ORIGIN – Body of Pubis, Inferior rami and outer surface of ramis of ischium. Magnus – Ischial tuberosity, Ramus of ischium
AT & R – Shld be done early, less than 4 years age. First adductor longus, then check correction required and do adductor brevis, only half. Here posterior branch of obturator nerve is der. If gracilis is tight, then release that also. Ant branch of Obturator nerve – Adductor longus, brevis and gracilis
Hips with contractures are more at risk. RISK - Flexion more than 20 degrees and abduct less than 30 degrees
Lateral position. DHS incision.
Medial – Adductor longus, brevis, gracilis Anterior approach – Inspect the head. If more than 50% cartilage is lost, then needs other procedures
Supine position. Lateral incision, 10cm superior gt and upto level of lt. Release all proximal femoral attachments nd make it free. Perform osteotomy. Seal the acetabulum with capsular edges, iliopsoas to lateral part of capsule and abductors to medial part. Close stump using vastus latralis.
Medially do adductor tenotomy. Laterally take incision and split gluteal muscles, iliopsoas tenotomy. Remove wt ver cartilage is left. Hip position - 40 degrees of flexion, 15 degree of abduction and neutral rotation.
These muscles include the rectus femoris anteriorly, gracilis medially, and semimembranosus, semitendinosus, and biceps femoris posteriorly A similar relationship exists between the knee and ankle with the gastrocnemius muscle, which crosses both joints
Knee flexed during stance phase leading to decreased stride length and increased energy expenditure. Spastic hamstrings or a week quadriceps can cause this.
If knee extension is limited as hip is flexed, then hamstring tightness is present. Medial hamstring tightness- Hips abducted, Knee flexed and off the table in supine position. If knee extension not possible without adduction then Medial hamstring tightness. Rectus femoris – Hip extended and knee off the table, patient is asked to extend knees. Spasticity of Rectus femoris – Pateint in prone position
Rectus femoris transfer – Supine, 5-6cm proximal to superior pole of patella.
High riding patella. ----- Meeting Notes (8/7/15 15:08) ----- patella index alta and baja.
Below soleal line, upper two thirds from post surface of tibia. Mainly into navicular
Incision – 5cm prox and medial to medial malleolus and extend distally over navicular. Release the tendon attachment. Make second incision 2cm proximal to lateral malleolus and extend till insertion of peroneus brevis (base of 5th MT) Pass TP through first incision to second and suture it to PB.
Insertion – Medial cuneiform and base of first MT, split the tendon. Second incision over the ant. aspect of leg at Tib ants musculo tendinous junction. Pull out the tendon from the second incision. Third incision, dorsal aspect of cuboid. Pass tendon into this incision and drill holes in cuboid and suture the tendon to itself.
Incision over lateral aspect of foot, 1cm posterior and inferior to peroneus longus tendon. Strip periosteum and cut wedge.
Collapse of medial longitudinal arch.
Sinus tarsi has talocalcaneal ligament. Incision – Anteriorly from middle of ankle and ending to peroneal tendons, obliquely over sinus tarsi. Excise fat from the sinus tarsi. Remove bone from it and and calcaneum to expose cancellous bone.
Lateral incision, protect peroneus tendon and do plantar fasciotomy and perform osteotomy using curved saw blade or osteotome. co
Ante-version – Axis of femoral neck and trans condylar axis of the knee.
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