cerebral palsy by dr hardev

1. CEREBRAL
PALSY
By: DR HARDEV SINGH
MODERATOR: DR SAMIR GROVER
Snr CONSULTANT
ORTHOPAEDIC

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

3. A Heterogenous Group of Movement Disorders
CEREBRAL PALSY
Three distinctive features common to all patients with cerebral palsy
:
(1) Some degree of motor impairment is present,
(2) An insult to the developing brain has occurred,.
(3) A neurological deficit is present that is nonprogressive,

4. In CP
• Muscles are unaffected
• Brain is unable to send
the appropriate
signals necessary to
instruct muscles when
to contract and relax

5. CAUSES
OF CEREBRAL PALSY

6. An insult or injury to the brain
–Fixed, static lesion(s)
–In single or multiple
areas of the motor
centers of the brain

7. • Development Malformations
– The brain fails to develop correctly.
• Neurological damage
– Can occur before, during or after delivery
* Unknown in many instances
CAUSES

8. Severe deprivation of oxygen or
blood flow to the brain
–Hypoxic-ischemic
encephalopathy
or intrapartal
asphyxia
CHIEF CAUSE

9. RISK FACTORS
• Prenatal factors
– Before birth
– Maternal characteristics
• Perinatal factors
– at the time of birth to 1mo
• Postnatal factors
– In the first 5 mos of life

10. Prenatal factors
1)Risk factors inherent to the
fetus (most commonly
genetic disorders),
2)Factors inherent to the
mother (seizure disorders,
mental retardation, and
previous pregnancy loss),

11. 3)Factors inherent to the pregnancy itself (Rh
incompatibility, polyhydramnios, placental rupture,
and drug or alcohol exposure).
4)External factors, such as TORCH (toxoplasmosis,
other agents, rubella, cytomegalovirus, herpes
simplex),

12. Perinatal Factors
1)Typically is associated with asphyxia or trauma
that occurs during labor.
2)Oxytocin augmentation,
3)Umbilical cord prolapse,
4)Breech presentation all have been associated
with an increased occurrence of cerebral palsy.
5)Cerebral palsy often is associated with low
Apgar scores during this period

13. Low-birth-weight infants (<1500 g) are at dramatically
increased risk of cerebral palsy.
This increased incidence is believed to be due to the
fragility of the periventricular blood vessels, which are
highly susceptible to physiological fluctuations during
pregnancy.

14. These fluctuations, which include hypoxic episodes,
placental pathology, maternal diabetes, and infection, can
injure these vessels and lead to subsequent intraventricular
hemorrhages.
Grading of Periventricular Lesions
I Bleeding confined to germinal matrix
II Bleeding extends into ventricles
III Bleeding into ventricles with dilation
IV Bleeding into brain substance

15. Postnatal Causes
Trauma, head injury
Infections
Lack of oxygen
Stroke in the young
Tumor, cyst

16. TYPES
OF CEREBRAL PALSY

17. Classification of CP
1.Geographical Classification1.Geographical Classification
2. Physiological Classification2. Physiological Classification

18. One extremity involved, usually lower
Monoplegia
Geographical Classification

19. Hemiplegia
In hemiplegia, one side of the body is involved, with
the upper extremity usually more affected than the
lower extremity.
Patients with hemiplegia, approximately 30% of
patients with cerebral palsy, typically have sensory
changes in the affected extremities as well.

20. Hemiplegia
limbs on only one side

21. • Hemiplegia on right side
–Hip and knee contractures
–Talipes equinus (“tip-toeing”
- sole permanently flexed)
–Asteriognosis may be present.
(inability to identify objects by
touch)

22. Diplegia
Diplegia is the most common anatomical type of
cerebral palsy, constituting approximately 50% of all
cases.
Patients with diplegia have motor abnormalities in
all four extremities, with the lower extremities more
affected than the upper.

23. The close proximity of the lower extremity tracts to
the ventricles most likely explains the more frequent
involvement of the lower extremities with
periventricular lesions .

24. Diplegia/ Paraplegia
•both legs•both legs w/ slight
involvement
elsewhere

25. Diplegia
May also have
Contractures of
hips and knees
and
talipes equinovarus
(clubfoot).

26. This type of cerebral palsy is most common in
premature infants
Intelligence usually is normal.
Most children with diplegia walk eventually,
although walking is delayed usually until around
age 4 years.

27. Quadriplegia
In quadriplegia, all four extremities are equally
involved, and many patients have significant
cognitive deficiencies that make care more difficult
Head and neck control usually are present, which
helps with communication, education, and seating.

28. Quadriplegia

29. Physiological Classification

30. 3 MAIN TYPES
1. PYRAMIDAL
- originates from the motor areas
of the cerebral cortex
2. EXTAPYRAMIDAL
- basal ganglia and cerebellum
3. MIXED

31. 4 MAIN TYPES
PYRAMIDAL 1. Spastic CP
EXTAPYRAMIDAL 2. Athethoid CP
3. Ataxic CP
MIXED 4. Spastic &
Athethoid CP

32. Spastic CP
• Increased muscle tone,
tense and contracted muscles
– Have stiff and jerky or
awkward movements.
– limbs are usually underdeveloped
– increased deep tendon reflexes
• most common form
• 70-80% of all affected

33. Spastic is the most common form of cerebral palsy,
constituting approximately 80% of cases, and usually is
associated with injury to the pyramidal tracts in the
immature brain.

34. Booth showed histologically that this altered muscle
function leads to the deposition of type I collagen in the
endomysium of the affected muscle, leading to thickening
and fibrosis, the degree of which correlated to the severity
of the spasticity.
Joint contractures, subluxation, and degeneration are
common in patients with spastic cerebral palsy.

35. • Spastic
Quadriplegia
Characteristic “scissors”
positions of lower limbs
due to adductor spasms.

36. Athetoid/ Dyskinetic CP
• Fluctuating tone
– involves abnormal involuntary
movements
– that disappear during sleep and
increase with stress.
– Interferes with speaking, feeding,
reaching, grabbing, and any other
skills
– 20% of the CP cases,

37. Athetoid cerebral palsy is caused by an injury to the
extrapyramidal tracts and is characterized by
dyskinetic, purposeless movements that may be
exacerbated by environmental stimulation.

38. Choreiform
Choreiform cerebral palsy is characterized by
continual purposeless movements of the
patient's wrists, fingers, toes, and ankles. This
continuous movement can make bracing and
sitting difficult.

39. Rigid
Patients with rigid cerebral palsy are the most hypertonic
of all cerebral palsy patients.
These patients have a “cogwheel” or “lead pipe” muscle
stiffness that often requires surgical release.

40. Ataxic CP
• Poor balance and lack of coordination
– Wide-based gait
– Depth perception usually affected.
– Tendency to fall and stumble
– Inability to walk straight line.
– Least common 5-10% of cases
Ataxic cerebral palsy is very rare
As a result of an injury to the
developing cerebellum.

41. 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.

43. MIXED CP
• A common combination is
spastic and athetoid
• Spastic muscle tone and involuntary
movements.
• 25% of CP cases, fairly common

44. Signs and
Symptoms
OF CEREBRAL PALSY

45. a.
b.
c.
d.
e.
f.
g.
h.

46. Early Signs
• Stiff or floppy posture
• Weak suck/ tongue thrust/
tonic bite/ feeding difficulties
• Poor head control
• Excessive lethargy or
irritability/ High pitched cry
Infancy (0-3 Months)

47. • Abnormal or prolonged
primitive reflexes
Moro’s reflex
Asymmetric tonic neck reflex
Placing reflex
Landau reflex
Early Signs

48. Late infancy
• Inability to perform motor skills as indicated:
– Control hand grasp by 3 months
– Rolling over by 5 months
– Independent sitting by 7 months
• Abnormal Developmental Patterns:
– Hand preference by 12 months
– Excessive arching of back
– Log rolling
– Abnormal or prolonged parachute response

49. Abnormal Developmental Patterns after 1
year of age:
• “W sitting” – knees flexed,
legs extremely rotated
• “Bottom shuffling” Scoots along the floor
• Walking on tip toe or hopping

50. Behavioral Symptoms
• Poor ability to concentrate,
• unusual tenseness,
• Irritability

51. ASSOCIATED
PROBLEMS
OF CEREBRAL PALSY

52. • Hearing and visual
problems
• Sensory integration
problems
• Failure-to-thrive, Feeding
problems
• Behavioral/emotional
difficulties,
• Communication disorders
• Bladder and bowel
control problems,
digestive problems
(gastroesophageal reflux)
• Skeletal deformities,
dental problems
• Mental retardation and
learning disabilities in
some
• Seizures/ epilepsy

53. Diagnosis
OF CEREBRAL PALSY

54. History and physical examination are the primary tools in
making the diagnosis of cerebral palsy.
The history should include a thorough investigation of the
pregnancy and delivery.
Ancillary studies, such as radiographs, hematological studies,
chromosomal analysis, CT, MRI, and positron emission
tomography, rarely are needed to make the diagnosis, but may
be helpful in determining the type and extent of cerebral palsy
present.

55. Diagnosis of cerebral palsy before age 2 years can be
very difficult.
Nelson and Ellenberg found that 55% of children
diagnosed with cerebral palsy by 1 year of age did not
meet the criteria by age 7 years.
Transient dystonia of prematurity is a condition
characterized by increased tone in the lower
extremities between 4 and 14 months old and often is
confused with cerebral palsy.

56. ASSESSMENT

57. CRITERIA
P osturing / Poor muscle control and strength
O ropharyngeal problems
S trabismus/ Squint
T one (hyper-, hypotonia)
E volutional maldevelopment
R eflexes (e.g. increaseddeep tendon)
*Abnormalities 4/6 strongly point to CP

58. Treatment
OF CEREBRAL PALSY

59. - No treatment to cure cerebral palsy.
- Brain damage cannot be corrected.
• Crucial for children with CP:
–Early Identification;
–Multidisciplinary Care; and
–Support

60. NON OPERATIVE TREATMENT
•
Commonly used as primary treatment or in
conjuction with surgery

Medication

Splinting

bracing

Physical therapy

61. MEDICAL MANAGEMENT
•
Common agents - diazepam
- baclofen
- dantrolene
- botulinum toxin

62. Oral agents:
Dantrolene-acts at the level of skeletal muscle and
decreases muscle calcium ion release. It has an
affinity for fast twitch muscle fibers and selectively
decreases abnormal muscle stretch reflexes and
tone.
Diazepam- increases inhibitory neurotransmitter
activity (GABA)
Baclofen -inhibit abnormal monosynaptic extensor
activity and poly synaptic flexor activity and
decrease substance P levels

63. Intrathecal injection of baclofen requires 1/30 the dose of
oral baclofen to achieve a similar or better response.
An implantable programmable pump dramatically decreases
the dose required to affect spasticity and decreases some of
the side effects such as sedation. This pump typically is
implanted subcutaneously in the abdominal wall and requires
refilling approximately every 2 to 3 months.

64. •
-intrathecal baclofen injection

65. 
Botulinum toxin type A (BTX-A) (Botox, Dysport) has
been used to weaken muscles selectively in patients with
cerebral palsy.

BTX-A injected directly into the muscle acts at the level
of the motor end plate, blocking the release of the
neurotransmitter acetylcholine and inhibiting muscle
contraction

This effect begins approximately 24 hours after
injection and lasts 2 to 6 monthsCare
– Intra muscular botulinum toxin for 2-6 months
– Safe maximal dose 36-50 U/kg

66. Physical therapy
Physical therapy typically is used as a primary treatment
modality and in conjunction with other modalities, such as
casting, bracing, BTX-A, and surgery.
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 cerebral
palsy include ankle-foot orthoses, hip abduction braces, hand
and wrist splints, and spinal braces or jackets.

68. Ankle foot orthosis

69. Floor reaction AFO
•
Uses floor reaction force through toe aspect of
foot plate to prevent forward tibial progression
& subsequent knee collapse
•
May be articulated

70. Knee brace

71. Ankle-foot-knee orthrosis

72. Abduction spint

73. Assisted Gait Trainer

74. Walking aids
•
Axillary crutches
•
Elbow crutches
•
Walking sticks

75. SURGICAL
MANAGEMENT

76. Operative Treatment
Operative treatment typically is 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.

77. Selective posterior rhizotomy
In some cases nerves need to be severed to decrease
muscle tension of inappropriate contractions.

78. How it Works
• The sensory nerve fibers in the spinal cord, usually
between the bottom of the rib cage and the top of the
hips are divided
• The nerve fibers are then stimulated and the
responses of the leg muscles are observed.
• Those that have an abnormal or excessive response
are severed.
• Those with a normal response are left intact.
• Intensive rehabilitation is required after the surgery,
usually up to six weeks, followed by physical therapy
on an ongoing basis

79. OPERATIVE MENAGEMENT HIP
•
Indications
•
contracture or deformities causing
pain
Decrease function
Interfere with ADL

80. PREREQUISITES FOR EFFECTIVE
SURGERY
•
hemiplegics / diplegics : good results
quadriplegics : minimal improvement
•
Age : 3- 12 years
•
IQ : good
•
Good upper limb function : for walking
•
Underlying muscle power should be good
•
surgery hardly changes status in
walkers/nonwalker, but improves gait

81. PROCEDURE
•
Neurosurgical procedures
•
Tendon release
•
Muscle tendon lengthening
•
Capsulotomies
•
Osteotomies
•
Resection and replacement procedures

82. DEFORMITIES
•
DEFORMITIES OF HIP:
•
Flexion deformities
•
adduction
•
Subluxation and dislocation
SECODARY DEFORMITIES:
•
Knee Flexion
•
Equinus foot
•
Pelvic tilt
•
Scoliosis and lordosis

83. •
Pseudoadduction
deformity

Flexion internal rotation
of hip

Incresed femoral
anteversion

External tibial torsion

Planovalgus feet
Pt sit in the ‘W’ position

84. Migration index (MI) is calculated
by dividing width of uncovered
femoral head A by total width of
femoral head B

85. Hip flexion
deformity

86. Indication for surgery
•
Hip flexion deformity never decrease by
physiotherapy.
•
Hip flexion deformity > 20 needs surgery

87. Hip flexion contracture hip , knee & ankle contracture
single stage
15-30 deg flexion >30 deg flexion multi level correction
ilioPsoas lengthening more release of
-rectus femoris
-sartorius
-TFL
-anterior fibers of Gl.minimus
Gl.medius

88. •
Iliopsoas recession is most commonly used
than complete tenotomy to avoid excessive
flexion weakness

89. ADDUCTION DEFORMITY

90. •
Mild contracture severe contractures
Early hip subluxation
Adductor tenotomy more release of
-gracilis
-anterior
half of
adductor bevis
•
Leave adductor brevis ( the major hip stabilizer )

91. HIP SUBLUXATION
•
MI > 30 % Soft tissue release for very young
Flexion adduction deformities
•
MI > 50% open reduction + femoral osteotomy
Correction of femoral valgus and anteversion
•
AI > 25 deg pelvic osteotomy
(Correction of acetabular deformities)

92. •
Femoral varus and derotational(external
rotation) osteotomy
•
Acetabular osteotomies:
•
Salter osteotomyredirection of the
acetabulum anterioly and laterally
•
Postero-superior deficiencyshelfs
osteotomy

93. HIP DISLOCATION
•
MI=100%
Types:
•
Posterior dislocation (m.c)
•
Anterior dislocation
Seen in
-spastic diplegics
-spastic quadriplegics

94. TRETMENT OPTIONS IN HIP
DISLOCATION
•
Observation
•
Relocation procedure on femur and
acetabulum
•
Proximal femoral resection
•
Hip arthrodesis
•
Total hip arthroplasty

95. Spastic Diplegia Spastic quadriplegia

96. hip dislocation :
if detected early: surgery
if detected late : no pain – leave
pain – proximal resection

97. Combined one stage correction of
spastic dislocated hip
1. Soft tissue release
2. Open reduction
3. femoral osteotomy
4. Pericapsular pelvic osteotomy

98. Varus derotational shortening
femoral osteotomy

99. Pericapsular acetabuloplasty

102. PROXIMAL FEMORAL RESECTION

103. FOOT
The most common deformity is ankle
equinus, with equinovarus and
equinovalgus deformities being equally
common.

104. Equinus Deformity
Equinus deformity is the most common foot deformity in
patients with cerebral palsy, affecting 70% of children.
Surgical Correction of Equinus Deformity
Open Lengthening of the Achilles Tendon
Z-Plasty Lengthening of the Achilles Tendon
Percutaneous Lengthening of the Achilles Tendon
Lengthening of the Gastrocnemius-Soleus Muscle

109. Equinovarus Deformity
Varus deformity, which usually is accompanied by
equinus, is caused most commonly by an abnormal
posterior tibial muscle that is overactive or firing out
of phase.
Lengthening of the Posterior Tibial Tendon
Z-Plasty Lengthening of the Posterior Tibial Tendon
Step-Cut Lengthening of the Posterior Tibial Tendon

110. Musculotendinous Recession of the Posterior
Tibial Tendon

111. Osteotomy of the Calcaneus

112. Equinovalgus Deformity

113. Medial Displacement Calcaneal Osteotomy

114. Subtalar Arthrodesis

115. KNEE
Flexion Deformity
Flexion is the most common knee deformity in patients with
cerebral palsy and frequently occurs in ambulatory children
Spastic hamstrings, weak quadriceps, or a combination of both
can cause isolated knee flexion.
Fractional Lengthening of Hamstring Tendons
Combined Hamstring Lengthening, Posterior Capsular Release,
and Quadriceps Shortening
Distal Transfer of Rectus Femoris

116. Than
k you