This document provides information on cerebral palsy (CP), including its definition, classification, causes, symptoms, and treatment approaches. CP is a non-progressive brain injury early in life that results in impaired motor function. It is classified based on the type of movement abnormality (e.g. spastic, athetoid) and the parts of the body affected (e.g. hemiplegia, diplegia). Common causes include prenatal infections, complications during birth like hypoxia, and postnatal infections. Treatment involves physical therapy, bracing, medication to reduce spasticity, botulinum toxin injections, and surgery to correct musculoskeletal deformities. The goals are to improve motor function, prevent

1. CEREBRAL PALSY
Dr. REJUL K RAJ
Dept. of Orthopaedics
CMCH LUDHIANA

2. INTRODUCTION
• first described by William Little in 1862.
• correlated the findings seen in young children
• associated them with difficult births.
• The term cerebral palsy originated with Freud.
• Static encephalopathy

3. DEFINITION
• wide variability in the manifestations
• CP was proposed as “a group of permanent
disorders of the development of movement
and posture, causing activity limitation, that
are attributed to non-progressive
disturbances that occurred in the developing
fetal or infant brain.”

4. In all cases, the following must
be true:
1. CP is the result of a brain lesion; therefore,
the spinal cord and muscles are structurally
and biochemically normal.
2. The brain lesion must be fixed and
nonprogressive. Thus, all the progressive
neurodegenerative disorders are excluded
from the definition.
3. The abnormality of the brain results in motor
impairment.

5. EPIDEMIOLOGY
• The incidence of CP is increasing slightly.
• 2.4 and 2.7 per 1000 live births.
• increased survival of low birth weight babies.
• whereas the rate of CP in infants of a given birth
weight has remained stable.
• Economic impact

6. ETIOLOGY
1. Prenatal
1. INFECTIONS.
The brain of the fetus is susceptible to
damage from maternalinfections and toxins.
The TORCHES group of infections
(toxoplasmosis, rubella, cytomegalovirus,
herpes, and syphilis) is known to cause
significant damage to the developing brain of
the fetus.
• Orthopaedic deformities in 82%.

7. 2. Cocaine, heroin, and marijuana and alcohol.
3. Rhesus blood group incompatibility-Kericterus.
4. Placental abnormalities,Renal failure etc.
• Fetal biophysical profile scores.
– high-risk pregnancies.
– antenatal hypoxia
– increased incidence of CP

8. 2. Perinatal.
1. Anoxia
1. A tight nuchal cord or placental abruption.
2. Fetal hypoxia may be detected by fetal heart rate
monitoring, but changes consistent with hypoxia,
such as late deceleration of the heart rate with
uterine contractions, are common and not specific
2. Premature delivery
3. Sepsis
4. Cardiac conditions.

9. 3. Postnatal
1. Infections such as meningitis in early childhood.
2. Hypoxia
1. Cardiopulmonary arrest,
2. near-drowning, and
3. Suffocation
3. Trauma
1. motor vehicle accidents
2. producing head injury
3. severe falls
4. child abuse

10. CLASSIFICATIONS
i. Physiologic
ii. Geographical.
iii. Functional.

11. I. Physiologic
• TYPE of movement disorder present.
1. Spasticity.
2. Hypotonia.
3. Dystonia.
4. Athetosis.
5. Ataxic

12. 1. SPASTICITY
• Most common
• damage to the pyramidal system, particularly the
motor cortex in the brain.
• Disinhibition of pathologic reflex arcs
• increased tone in the extremities.
• The tone is dependent on velocity, which means that
if a muscle is stretched rapidly, tone increases more
than if the same muscle group were stretched
gradually and gently.
• ‘CLASPED KNIFE DEFORMITY’.

13. 2. HYPOTONIA
• abnormally decreased tone.
• described as floppy or hypotonic.
• usually a phase and most frequently
• leads to spasticity as the infant matures.

14. 3. DYSTONIA
• is described as increased tone,
• which is not dependent on velocity.
• tone in dystonic CP is described as “LEAD
PIPE” which means that tone does not
decrease with gentle prolonged stretching.

15. 4. ATHETOSIS
• is characterized by abnormal writhing
movements that the patient cannot control.
• exaggerated as the patient tries to complete a
purposeful motion.
• basal ganglia.
• Speech - difficult to understand
• neonatal kernicterus.

16. 5. ATAXIC
• Cerebellar lesions lead to ataxic CP.
• wide-based and clumsy gait.
• rare.

17. “It is important to correctly classify the
movement disorder of a patient with CP
because the results of surgical treatment are
unpredictable for all but purely spastic
patients.”

18. II. GEOGRAPHIC
• Part of the body affected,
1. Hemiplegia
2. Diplegia –
- With both lower extremities being involved
(though not always symmetrically) and lesser
involvement of the upper extremities
3. Triplegia
4. Quadriplegia

22. III. FUNCTIONAL
• Current emphasis.
• The Gross Motor and Functional
Classification System (GMFCS)
• Five levels.

24. • level 1 - 34.2%
• level 2 - 25.6%
•
• level 3- 11.5%
• level 4- 13.7%
• level 5- 15.6%

25. EVALUATION - HISTORY
• Birth history – Birth weight, gestational age,
complications, NICU, entilator etc.
• Motor Mile stones- Delayed.
• Preferential use of one hand or leg.
• strabismus, difficulty swallowing, frequent
choking, delayed speech development, poor
eyesight, and seizures ( 20 to 40 %)
Head control 3 to 6 months
Sitting 6 to 9 months
Crawling 9 months
Standing and cruising 10 to 12 months
Walking 12 and 18 months

26. PHYSICAL EXAMINATION
1. Muscle tone –
• Spasticity feels like tightness in the muscles,
which become tighter the quicker the limbs
are passively moved.
• Greater range of motion can be gained by
slowly and gently stretching the joints in
question.

27. • Tardieu test is a measure of spasticity.
• For example, if the examiner is assessing
hamstring spasticity, the angle at which a
“grab” of resistance occurs when quickly
extending the knee with the hip in flexion is
compared with the amount of extension
possible when the knee is stretched.
• Difference in angle is the spasticity.

28. 2. Deep tendon reflexes
– are increased in patients with CP
– Clonus
– Asymmetric in hemiparesis.
– Infantile reflexes will be retained.
3. Balance, Sitting, and Gait
– Crouched gait
– Toe walking with Genu Recurvatum
– Jumping gait
– High stpping gait.
– Scissoring gait.

31. HPE + IMAGING
1. periventricular leukomalacia
2. intraventricular and periventricular
hemorrhage.
Patchy areas of necrosis secondary to
vascular insult

32. TREATMENT
“the child with cerebral palsy becomes the
adult with cerebral palsy.”
- Rang

33. • Childhood is the optimal time for intervention
to maximize the function of a patient with CP.
• duty to ensure that the musculoskeletal
treatment of the child prevents future
problems with pain and deformity as an adult.
• Patients with CP do not usually have severely
shortened life spans.

34. NON SURGICAL TREATMENT-
1.PHYSICAL THERAPY.
• Frequently the first treatment.
• Yet no controlled studies have confirmed.
• Passive stretching.
• Strenghtening of the muscles.
• Wheel chair transfers.

35. 2. ORTHOSIS
• Improving gait in ambulatory
• AFOs are helpful in positioning the ankle and
foot during gait.

36. Indications for bracing
1. To obtain a plantigrade foot position and reduce
genu recurvatum in patients with dynamic equinus.
• 2. To support the foot in dorsiflexion during swing
phase when footdrop is present
• 3. To assist the foot postoperatively while weakness is
being treated by physical therapy.
• 4. To improve mild crouch

38. CONTRAINDICATIONS
• Nonambulatory patients who are able to wear
shoeswith orthoses- Level 4 and 5.
• Preambulatory
– they interfere with the child’s ability to crawl and
move about the floor.

39. 3. MEDICAL THERAPY
• ORAL.
– Diazepam , Baclofen, Tizanidine
– reduce tone, relieve spasticity
• Intrathecal Baclofen.
– a -aminobutyric acid agonist, acts at the spinal
cord level to impede release of the excitatory
neurotransmitters that cause spasticity

40. Botulinum Toxin
• Clostridium botulinum
• blocking the release of acetylcholine at the NMJ
• The targeted muscle becomes weak because of lack of
innervation until the neuromuscular junction sprouts new
endings.
• dynamic deformities in the absence of fixed contracture.
• begins taking effect after 2 to 3 days
• wears off after approximately 3 months

41. Indications
1. A child with a dynamic equinus deformity
and no fixed plantar flexion contracture
2. A child with equinus gait without multilevel
crouch
3. A child younger than 4 years who cannot
tolerate AFOs because of dynamic equinus
4. Parents’ desire for injections and refusal of
tendonlengthening surgery

42. SURGERY- GENERAL PRINCIPLES
• Goals of the surgery – defined and discussed.
• Once other modalities fail.
• Expected Post operative course.
• NO CURE.
• “Walk differently hopefully better but no normal “.

43. SURGERY – TIMING.
• combining multiple tendon surgeries and
osteotomies into a single surgical event (SEMLS).
• Single Event Multi Level surgery.
• Avoid ‘ birthday surgery ‘.
• correcting all concomitant contractures
simultaneously during one surgery is important
to avoid recurrence or overcorrection.

44. • Because gait changes and matures until
approximately 7 years of age
• Hip subluxation
• progress has been halted by contractures
• Adductor release for scissoring and hamstring
lengthening

45. MANAGEMENT OF FOOT
1. EQUINUS
2. EQUINOVARUS
3. PES VALGUS
4. ANKLE VALGUS
5. BUNIONS

46. 1. EQUINUS

47. Silfverskiöld test
• If the ankle can be passively dorsiflexed with
the knee bent to 90 degrees but cannot be
dorsiflexed with the knee extended,
• it is believed that the gastrocnemius is tight
but the soleus is not contracted

49. • Selective lengthening of the Achilles tendon or
gastrocnemius fascial recession or aponeurotic
release.
• that gastrocnemius recession should be
performed when,
• Silfverskiöld test performed under anesthesia
is positive and

50. Treatment options
1. Physical therapy.
– Stretching.
– Inhibition casts.
2. Orthotics
– AFOs
3. Myoneural blocks.
4. Surgical

51. Surgery.
1. Isoloated Gastrocnemius – Aponeurotic
lenghtening.
2. Gastocnemius + Soleus – TA Lenghtening
3. Don’t over lengthen – calcaneal deformity.
4. Aponeurotic lengthening is preferred over TA

52. Gastrocnemius recession-
Strayer, Baker, or Vulpius
• Vulpius procedure –
– the aponeurosis of the gastrocsoleus is divided in chevron fashion
– the midline fibrous septum of the soleus is transected,
– but the soleus muscle fibers are not disturbed
• Strayer procedure-
– The cut in the gastrocnemius is transverse and more proximal
– not lengthen the soleus whatsoever
• Baker technique –
– the gastrocsoleus aponeurosis is cut in tongue-in-groove fashion and
– dissected free from the underlying soleus muscle.
– The fascia is allowed to slide on the underlying muscle, thereby increasing the
overall length of the muscle,
– and the four corners of the aponeurosis are
– sutured in the lengthened position

58. 2. EQUINOVARUS DEFORMITY
• Muscle imbalance in which the invertors of the foot,
specifically the, posterior and anterior tibialis muscles,
overpower the evertors (the peroneals).
• The gastrocnemius contributes equinus to the
deformity.
• Patients walk on the lateral border of the inverted foot,
• painful calluses may develop laterally over the fifth
metatarsal.

60. If supination of the
forefoot is seen, the anterior tibialis is most
likely contributing
to the equinovarus deformity.
Next, feels for spasticity in the posterior
tibialis muscle.
Passive manipulation of the hindfoot into
valgus while feeling the posterior tibialis
tendon can help
the physician appreciate tightness in the
posterior tibialis

61. Surgery
• Split Tibialis anterior transfer.
• Split tibialis posterior transfer.
• Tenotomy of tibialis posterior.

66. 3. PES VALGUS

67. 4. HALLUX VALGUS

69. 5. ANKLE VALGUS

70. 6. BUNIONS

71. MANAGEMENT OF KNEE
• Flexion deformity of the Knee.
• Genu recurvatum.
• Stiff-knee gait.
– rectus femoris muscle transfer.

72. Problems
• Hamstring spasticity or contracture
• Quadriceps weakness
• Lengthening of the patellar tendon and patella
alta
• Flexion deformity

73. HARMSTRING SPASTICITY

77. Treatment
• PT (hamstring + quadriceps strengthening)
• Myoneural block of hamstring muscles.
• Floor-reaction orthosis.
• Hamstring release.
• Hamstring transfer.
• Femoral supracondylar extension osteotomy.
• Correcting patella alta
– Plication of the patellar tendon
– Distal transfer of the tibial tuberosity

78. HARMSTRING RELEASE
• The most widely recommended
• fractional lengthening technique.
• aponeurotic lengthening of the
semimembranosus and biceps femoris and Z-
plasty of the semitendinosus.

79. HARMSTRING TRANSFERS.

80. MANAGEMENT OF HIP
1. Adduction deformity
2. Flexion deformity
3. internal rotation gait
4. Hip subluxation and dislocation.

81. Problems – Adduction deformity
• Scissor gait
• Tendency for hip subluxation and dislocation
• Interference with perineal hygiene
• Recurrence of deformity
• Overcorrection of deformity

82. Treatment options for dealing with
adduction deformity and scissoring
• Stretching exercises and modification of sitting
and lying posture.
• Myoneural blocks.
• Adductor tenotomy and obturator neurectomy.
• Adductor transfer

83. Problems – Flexion deformity
• Abnormal posture and gait.
– hip flexion and compensatory knee flexion or
– with the knee straight and compensatory lumbar
lordosis
• Tendency for hip instability.
• Excessive weakening of the hip flexor

84. MANAGEMENT OF HIP

85. Treatment
• Stretching exercises- Hip flexors.
• Myoneural blocks- Iliopsoas.
• Iliopsoas tenotomy.
– Division of the iliopsoas tendon close to its
insertion into the lesser trochanter
• Intramuscular release of psoas at the pelvic
brim.
• Rectus femoris release

86. Treatment options - Internal rotation gait
• Femoral derotation osteotomy.
– due to femoral anteversion
• Medial hamstring release
• Anterior and medial transfer of gluteus
medius.
• Selective internal rotator release

87. References
• Tachdjian Pediatric Orthopaedics 5E .
• Benjamin Joseph. Paediatric Orthopaedics. A
system of decision making.

88. THANK YOU