Cerebral palsy is a heterogeneous disorder of movement and posture caused by a non-progressive brain injury early in development. It presents with a wide variety of motor impairments and can be classified anatomically (e.g. hemiplegia) or physiologically (e.g. spastic, athetoid). Risk factors include prenatal, perinatal, and postnatal insults. Treatment involves both non-operative measures like medication, bracing, and physical therapy as well as operative interventions like tendon lengthening and osteotomies to prevent or treat deformities when they interfere with function. Prognosis depends on the extent and location of brain injury.

1. Cerebral palsy
Presenter – Dr. Madhukar

2. Definition
• Cerebral palsy is a heterogeneous disorder of
movement and posture that has a wide
variety of presentations, ranging from mildly
affected individuals who present with some
degree of motor disturbance to severely
affected patients who have total body
involvement.

3. Etiology
• CP is believed to occur due to insult to the
brain between the time of conception and age
of 2 years.
• Although it can occur anytime before the age
of 8 years.
• After the age of 8, most of the development of
the immature brain is complete, as is gait
development.

4. • Although the neurological deficit is permanent
and nonprogressive, the effect it can have on the
patient is dynamic, and the orthopaedic aspects
of cerebral palsy can change dramatically with
growth and development.
• Growth, along with altered muscle forces across
joints, can lead to progressive loss of motion,
contracture, and eventually joint subluxation or
dislocation, resulting in degeneration that may
require orthopaedic intervention.

5. Risk factors
• Prenatal
- Fetus (genetic disorders)
- Mother (seizure disorders, mental
retardatoion, previous pregnancy loss)
- Pregnancy (Rh incompatability,
polyhydramnios, placental rupture, drug or
alcohol exposure)
- External factors (TORCH syndrome)

6. • Perinatal
- Asphyxia or trauma that occurs during labour
- Oxytocin agumentation
- Umblical cord prolapse
- Breech presentation

7. • Postnatal
- hypoxic-ischemic encephalopathy
- Meconium aspiration
- Persistant fetal circulation
- Infections ( encephalitis, meningitis)
- Trauma
- Child abuse

8. Classifications
• Geographical
- Monplegia
- Hemiplegia
- Diplegia
- Quadriplegia
- Double hemiplegia
- Total body

9. Physiological
• Pyramidal type or spastic type
• Extrapyramidal type which include Athetoid,
Choreiform, Ataxic, Rigid and Hypotonic.

10. Spastic
• Most common
• Velocity-dependent increased muscle tone
and hyperreflexia with slow, restricted
movement due to simultaneous contraction of
agonist and antagonist muscles.
• Joint contractures, subluxtions and
degenrations are common in this type.

11. Athetoid
• Characterized by dyskinetic,(constant succession
of slow, writhing, involuntary, purposeless
movement) that may be exacerbated by
environmental stimulation.
• In pure athetoid cerebral palsy, joint contractures
are uncommon.
• Dystonia, characterized by increased overall tone
and distorted positioning in response to
voluntary movements, or hypotonia also can
occur with athetoid cerebral palsy.

12. Choreiform
• Characterized by continual purposeless
movements of the patient’s wrists, fingers,
toes, and ankles.
• This continuous movements can make bracing
and sitting difficult.

13. Rigid
• Patients with rigid cerebral palsy are the most
hypertonic of all cerebral palsy patients.
• This hypertonicity occurs in the absence of
hyperreflexia, spasticity, and clonus, which are
common in spastic cerebral palsy.
• These patients have a “cogwheel” or “lead
pipe” muscle stiffness that often requires
surgical release.

14. Ataxic
• Ataxic cerebral palsy is very rare and probably is
the most often misdiagnosed type.
• It is characterized by the disturbance of
coordinated movement, most commonly walking,
as a result of an injury to the developing
cerebellum.
• It is important to distinguish true ataxia from
spasticity because with treatment many children
with ataxia are able to improve their gait function
without surgery.

15. Hypotonic
• Hypotonic cerebral palsy is characterized by
weakness in conjunction with low muscle tone
and normal deep tendon reflexes.
• Many children who ultimately develop spastic or
ataxic cerebral palsy pass through a hypotonic
stage lasting 1 or 2 years before the true nature
of their brain injury becomes apparent.
• Persistent hypotonia can lead to difficulties with
sitting balance, head positioning, and
communication.

16. Mixed
• Many patients with cerebral palsy have
features of more than one type and are
referred to as having mixed cerebral palsy.
• Patients with mixed cerebral palsy usually
show signs of pyramidal and extrapyramidal
deficits.
• The final clinical appearance is determined by
the relative components of spasticity,
athetosis, and ataxia.

17. • No one system is optimal for the classification
and description of patients with cerebral palsy
because of their heterogeneity.
• Because many patients exhibit variable patterns
of motor activity that do not fit completely into
one category or another, an individualized
approach should be used for each patient.
• Palisano et al. developed the Gross Motor
Function Classification System to help resolve
these classification difficulties

18. Gross Motor Function Classification System
• 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, cannot sit independently, is
dependent for all aspects of care

19. Diagnosis
• History
• Physical examination
• Gait analysis

20. Early signs
• Stiff or floppy posture.
• Excessive lethergy or irritability/ high pitched
cry
• Poor head control.
• Week suck/tongue thrust/tonic bite/feeding
difficulties

21. Physical examination
• It mainly consists of 7 main points
1. Strength and selective motor control of isolated
muscle.
2. Degree and type of muscle tone.
3. Degree of static muscle and joint contracture.
4. Torsional and other bone deformities.
5. Fixed mobile foot deformities.
6. Balance, equilibrium responses and standing
posture.
7. Gait by observation.

22. Gait analysis
• Observational
• Computerized

23. Observational gait analysis
• Beginning from the feet the following points must be
considered
- Position of the foot at the end of terminal swing
- Position of ankle
- Foot progression during stance and swing; position of
foot in stance phase.
- Alignment of forefoot with hindfoot; arch of foot; point
of gait cycle where deviation occurs from normal;
position of toes in swing and stance phases
- At knee, position of knee in terminal swing and initial
contact; max degree of flexion at in swing; varus/valgus
during stance.

24. • At pelvis; hip and trunk alignment of thigh to
line of progression, hip extension in terminal
stance; excessive
abduction/adduction(scissoring) in swing
phase, pelvis obliqutiy.
• Trunk movements in each plane, movement of
arms and wether child elevates his/her hands
for balance.

25. Computerized gait analysis
• Observational is more difficult proximally
where large muscles obscure hips and pelvis.
• Computerized gait analysis is helpful in
determining any deviations in these joints.

26. • Some common gait patterns in spastic diplegia
cp include:
• Jump-knee gait
• Toe-toe gait pattern
• Crouch gait
• Stiff knee gait
• Rotational deformities that affect gait (femoral
anteversion and tibial torsion)

28. Prognostic factors
• Poor prognostic signs for walking reported by Bleck
included
• (1) an imposable asymmetrical tonic neck reflex,
• (2) persistent Moro reflex,
• (3) strong extensor thrust on vertical suspension,
• (4) persistent neck-righting reflex, and
• (5) absence of normal parachute reflex after 11 months.
• The persistence of these primitive reflexes is associated
with extensive and severe brain damage and a poor
prognosis for independent ambulation, self-care, and
activities of daily living.

29. Associated conditions
• Mental impairment or learning disability
(40%)
• Seizures (30%)
• Complex movement disorders (20%)
• Visual impairment (16%)
• Malnutrition and related conditions like
GERD(15%)
• Hydrocephalus (14%)

30. Treatment
• Non-operative
• Operative

31. Non-operative
• This includes modalities such as
- Medication
- Splinting and bracing
- Physical therapy

32. Mediacal
• Commonly used 4 types
- Benzodiazepines (Diazepam)
- Baclofen
- Dantrolene sodium
- Botox

33. • Diazepam acts by facilitating transmission at the
inhibitory synopsis in the CNS called GABBA
receptors.
• Reduces mono and poly-synaptic reflexes
resulting in increased inhibition, there by
reducing the spasticity.
• Acts both on brain and spinal chord.
• Most common Side effect is sedation and develop
tolerance or dependence.
• Dosage – 0.12 to 0.8 mg/kg/day

34. • Baclofan is a structural analog of GABBA and
binds to GABBAb receptors resulting in
inhibition of mom and poly-synaptic reflexes.
• Acts mainly on spinal chord.
• Reduces spasticity, hyperreflexia and clonus.
• Dosage – 2.5mg – 10mg/day upto 40mg a day
in divided doses.

35. • Baclofan has a poor BB barrier penetration
and has short half-life (3-4hrs)
• Hence requires gradual titration and use of
extremely high systemic levels to obtain a
central effect of spasticity reduction.
• Intrathecal injection requires 1/30 the dose of
oral baclofan to achieve same result.

36. • Implantable programmable pump is used in
injecting balofan intrathecally.
• Implanted subcutaneously in abdominal wall.
• Refill in 2-3months.

37. • Dantrolene sodium acts at the site of skeletal
muscles as opposed to other drugs which act
on the neurotransmitter system.
• It acts by inhibiting the release of calcium ions
from sarcoplasmic retinaculium during muscle
contractions.
• Reduces clonus and muscle spasms.
• Dosage – 6-8mg/kg/day in divided doses.

38. • Botulinum toxin is an effective synaptic blocker
which acts on inhibition of release of
acetylcholine at the presynaptic junction.
• Produced by clostridium botulinum.
• Two serotypes available in market A and B.
• A – BOTOX, B – MYOBLOC.
• Effects are reversible hence required every 2-
3months
• Dosage – 10-12U/kg but not > 400U

39. Splinting and bracing
• Bracing in patients with cerebral palsy most
commonly is used to prevent or slow
progression of deformity.
• The most commonly used braces for the
treatment of cp include AFO, hip abduction
braces, hand and wrist splints and spinal
braces or jackets.

41. Operative treatment
• Indicated when contractures or deformities
decrease function, cause pain, or interfere
with activities of daily living.
• It is the only effective treatment when
significant fixed contractures exist.
• Should be scheduled to minimize the number
of hospitalizations and interference with
school and social activities.

42. • “Birthday surgery” or multiple procedures
performed at different times, as described by
Rang, should be avoided whenever possible.
• The use of single-event multilevel surgery has
been shown to improve both upper and lower
extremity function as well as quality of life
while minimizing a patient’s exposure to
repeated hospitalizations and rehabilitation.

44. NEUROSURGICAL INTERVENTION
• Selective dorsal root rhizotomy is a technique to reduce
spasticity and balance muscle tone in carefully selected
patients.
• In patients with cerebral palsy, the normal central nervous
system inhibitory control of the gamma efferent system is
deficient, leading to the exaggerated stretch reflex
response.
• Goal is to identify the rootlets carrying excessive
stimulatory information and section them to reduce the
stimulatory input from the dorsal sensory fibers.
• The ideal patient - 3 to 8 years old with spastic diplegia,
voluntary motor and trunk control, pure spasticity, and no
fixed contractures.

45. SELECTIVE POSTERIOR RHIZOTOMY

46. Hip
• In most patients, the hip is normal at birth and
radiographic changes typically become apparent
between 2 and 4 years of age.
• The cause of this progressive deformity is multifactorial
and includes muscle imbalance, retained primitive
reflexes, abnormal positioning, and pelvic obliquity.
• These altered forces across the hip along with
decreased weight bearing lead to bony deformities,
including acetabular dysplasia, excessive femoral
anteversion, increased neck-shaft angle, and
osteopenia.

47. Migration index

48. Flexion deformities at hip

49. Adduction deformity at hip
• Most common in cp
• This can cause various deformities like
scissoring gait, hip subluxations.
• Surgery- adductor tenotomy
and release.
Indicated in mild contractures and
should be done as early before 4yrs
can be done till 8yrs.

50. Adductor tenotomy and release

51. Varus derotational osteotomy
• Indicated for patients with excessive
anteversion and valgus deformity of the
proximal femur and a hip that is either
subluxated or dislocated.
• Resection arthroplasty, arthrodesis, THA are
proposed in painful dislocated hip when a
relocation procedure is not possible.

53. Proximal femur resection

54. Knee
• Deformities of the knee in patients with cerebral palsy are
difficult to evaluate and treat and rarely occur in isolation.
• Pelvic, hip, knee, ankle, and foot deformities are
interrelated. The hip and the knee are tightly coupled
because of the muscles that cross both joints, the “two-
joint muscles.”
• Pathological conditions that affect these muscles, such as
spasticity or contracture, and surgical changes affect the
function of both joints.
• Hence a careful physical examination of the entire lower
extremity is essential when evaluating the knee in patients
with cerebral palsy.

55. • Commonly seen deformities at knee are
1. Felxion deformity
2. Recurvatum of knee
3. Knee valgus
4. Patella alta

56. Flexion deformity of knee
• Knee flexion deformities keep the knee from
fully extending at the end of the swing phase
of gait.
• This causes the knee to be flexed during
stance phase, leading to decreased stride
length and increased energy expenditure
• Can result from hip or ankle pathology.

57. • Patients with spastic hip flexors or weak hip
extensors or both develop compensatory knee
flexion that results in crouch gait in which the
hips, knees, and ankles are flexed.
• To find the source of the knee flexion, the
muscles must be assessed to determine if the
deformity is caused by spasticity or
contracture or both.

58. FRACTIONAL LENGTHENING OF
HAMSTRING TENDONS

59. • Other techniques
- Combined hamstring lengthening , posterior
capsular release
- Distal femoral extension osteotomy and
patellar tendon advancement.
- Distal transfer of rectus femoris.

60. Distal transfer of rectus femoris

61. Foot
• Equinus deformity
• Equinovarus deformity
• Equinovalgus deformity
• Calcaneus deformity
• Cavus deformity
• Forefoot adduction deformity
• Hallux- valgus deformity
• Claw toes.

62. Equinus deformity

64. Equinovarus deformity
• Lengthening of posterior
tibial tendon
- z-plasty
- Step-cut lengthening
- Musculotendinous
recession
• Split tendon transfers
- Posterior tibial tendon
- Anteriot tibial tendon
• Osteotomy of calcaneus

65. Equinovalgus deformity
• Medial displacement calcaneal osteotomy.
• Subtalar arthrodesis.

66. Cavus deformity
• Crecentric osteotomy of calcaneus.

67. Thank You.