Cerebral palsy is a nonprogressive, permanant musculo skeletal anomaly due to ischemic disease during birth.

1. CEREBRAL PALSY
Dr. NAVEEN RATHOR
Dept. of Orthopaedics
RNTMC , UDAIPUR

2. CEREBRAL
PALSY
• A motor function disorder
– caused by permanent, non-progressive brain lesion
– present at birth or shortly thereafter. (Mosby, 2006)
• Non-curable, life-long condition
• Damage doesn’t worsen
• May be congenital or acquired

3. 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. Although brain lesions that result in CP are not
progressive, clinical picture of CP may change with
time due to devlopment of muscle and joint
contracture.

4. 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

5. ETIOLOGY-Severe deprivation of oxygen or
blood flow to the brain
A. Prenatal ( 70 % )
1.INFECTIONS-The TORCHES group of infections
2.Rhesus blood group incompatibility
3.Kericterus.etc
B. Perinatal (5-10 % )
1. FETAL Anoxia
2. Premature delivery
3. Sepsis
4. Cardiac conditions.
C. Postnatal
1. Infections such as meningitis in early childhood.
2. Hypoxia
3. Trauma

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

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

8. 1. SPASTICITY
• Most common
• damage to the pyramidal system, particularly the
motor cortex (corticospinal tract ) 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’-decerase in resistence
when it is passively flexed.

9. 2. DYSTONIA
• is described as increased tone,
• Due to lesion in basal ganglia.
• 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.

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

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

12. “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.”

13. 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
-m/c form of cerebral palsy
3. Double hemiplegia
4. Quadriplegia
5. Monoplegia-rare

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

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

17. EVALUATION - HISTORY
• Birth history – Birth weight, gestational age,
complications, NICU 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

18. 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.

19. • 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.

22. 2. Deep tendon reflexes
– are increased in patients with CP
– Clonus
– Asymmetric in hemiparesis.
– Infantile reflexes will be retained.
3. Balance, Sitting, and Gait
Gait analysis-observational
computerised
instrumental
– Crouched gait
– Jumping gait
– High stpping gait
– Scissoring gait
– True and apperent equinus

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

25. MANAGMENT
• 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.

26. NON SURGICAL TREATMENT-
1.PHYSICAL THERAPY.
• Frequently the first treatment.
• Passive stretching.
• Strenghtening of the muscles.
• Wheel chair transfers
2. ORTHOSIS
-Improving gait in ambulatory
-AFOs are helpful in positioning the ankle and foot
during gait.

27. 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

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

29. 3. MEDICAL THERAPY
• Dantrolene sodium-peripheral acting muscle
relexent
-act by inhibiting calcium ion release during
muscle contraction.
-Diazepam , Baclofen, Tizanidine
– reduce tone, relieve spasticity

30. Intrathecal Baclofen
a -aminobutyric acid agonist, acts at the spinal
cord level to impede release of the excitatory (
GABA) neurotransmitters that cause spasticity

31. Botulinum Toxin
• Botulinum toxin type A commonly marketed at BOTOX.
• 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

32. 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 tendon
lengthening surgery.

33. 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 “.

34. SURGERY – TIMING.
• combining multiple tendon surgeries and
osteotomies into a single surgical event, Single
Event Multi Level surgery (SEMLS).
• Avoid ‘ birthday surgery ‘- correcting all
concomitant contractures simultaneously during
one surgery is important to avoid recurrence or
overcorrection. Because gait changes and matures
until approximately 7 years of age.

36. Selective Dorsal Rhizotomy
• Neurosurgical intervention
• A technique to reduce spasticity and balance muscle
tone in carefully selected patients.
• The goal of selective dorsal rhizotomy 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 for this procedure is a child 3 to 8 yr
old with spastic diplegia , voluntary motor and trunk
control, pure spasticity, and no fixed contractures.
• Majority of patients can be expected to improve one
GMFCS level.

37. INDICATIONS-
-The ideal patient for this procedure is a child 3 to 8 yr
old with spastic diplegia , voluntary motor and
trunk control, pure spasticity, and no fixed
contractures.
Complication-
-hip subluxation and dislocation
-lumber lordosis , scoliosis ,spondylosis and
spondylolisthesis
-paraparesis

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

39. 1. EQUINUS
-One of the m/c deformity.
-m/c due to calf muscle spasticity (hamstring
contracture).
-should be deferentiated from apperent equinus.

40. Silfverskiöld test –for hamstring contracture
• 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.

42. Gastrocnemius recession-
Strayer, Baker, or Vulpius
• Strayer procedure-
– The cut in the gastrocnemius is transverse and more
proximal
– not lengthen the soleus whatsever

43. • Baker technique –
– the gastrosoleus 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

44. Vulpius procedure –
the aponeurosis of
the gastrocsoleus is
divided in chevron
fashion
the midline fibrous
septum of the
gastronemius is
transected,
but the soleus
muscle fibers are
not disturbed .

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

48. 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 gastronemius contributes equinus to the
deformity.
• Patients walk on the lateral border of the inverted foot,
• painful calluses may develop laterally over the fifth
metatarsal.

50. 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

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

52. Management of knee-
Problems
• Hamstring spasticity or contracture
• Quadriceps weakness
• Lengthening of the patellar tendon and patella
alta
• Flexion deformity

53. HARMSTRING SPASTICITY

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

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

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

58. Problems – Adduction deformity
• Scissor gait
• Tendency for hip subluxation and dislocation
• Recurrence of deformity
• Overcorrection of deformity

59. 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

60. Adductor tenotomy
identify the adductor longus by palpation, and make a 3 cm
transverse incision over the adductor longus tendon
approximately 1 cm distal from its origin.

61. 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

62. Treatment
• Stretching exercises- Hip flexors.
• 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

63. Iliopsoas
recession
make a 5cm incision medial
to and 2 cm below the
ASIS.
Develop the interval
between the tensor fascia
lata and sartorius.
Palpate the pelvic brim just
medial and inferior to the
rectus femoris origin to
locate the iliopsoas tendon
in a shallow groove.

64. Treatment options - hip subluxation and
dislocation (Internal rotation gait)
• Femoral varus and derotation osteotomy.
• Medial hamstring release
• Anterior and medial transfer of gluteus
medius.
• Selective internal rotator release

65. Varus femoral derotation osteotomy of hip

67. THANK YOU FOR PATIENTLY LISTENING!!!
"Time and gravity
are enemies of very aging body,
especially mine." - Adult with CP