1. Cerebral Palsy

Dr Surya Kumar

2. Cerebral Palsy = Brain Paralysis
Definition
Prevalence
Etiology
Classifications
Clinical Presentation
Treatments
Substantially Disabling

3. Cerebral Palsy: Definition
Cerebral palsy is a static encephalopathy
Encephalopathy = Brain Injury that is non-
progressive disorder of posture and movement
Variable etiologies
Often associated with epilepsy, speech problems,
vision compromise, & cognitive dysfunction

4. LATEST DEFINITION OF CEREBRAL PALSY
“Cerebral palsy describes 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. The motor disorders of cerebral palsy are often
accompanied by disturbances of sensation, perception,
cognition, communication and behavior, by epilepsy, and by
secondary musculoskeletal disorders”
Rosenbaum P et al: Dev Med Child Neurol (Suppl.) 2007;109:8-14

5. Cerebral Palsy: Classification
Various classifications of Cerebral Palsy
Physiologic
Topographic
Etiologic

6. Cerebral Palsy: Physiologic
Athetoid
Ataxic
Rigid-Spastic
Atonic
Mixed

7. Cerebral palsy
Classification
According to Pattern of involvement
Monoplegia : one limb / rare
Diplegia : both LL >> UL / good intelligence /
prematurity
Hemiplegia : unilateral usually UL > LL / 33 % seizures
50 % mentally retarded
Triplegia : rare / usually both LL + one UL
Quadriplegia : total body / often mentally retarded /
with seizures / severe hypoxia
Double hemiplegia : bilateral UL > LL

8. Cerebral palsy
Classification
According to Type of motor dysfunction
Spastic 65 %
Athetoid 10 %
Ataxic 5 %
Mixed 12 %
Hypo tonic 1 %

9. Gross motor functional classification system
Level Function
I Ambulatory in all settings
II Walks without aides but has
limitations in community settings
III Walks with aides
IV Mobility requires wheelchair or adult
assist
V Dependent for mobility

10. Etiology
Prenatal – 70 to 80 %
Natal - Upto 10 %
Rest postnatal
Upto 5 year ? ( Veena kalra AIIMS)

11. “ASPHYXIA” AND CP IN THE NCPP STUDY
2 3 C H IL D R E N
W IT H O T H E R R E A S O N S F O R C P
1 2 < 2 K G , 1 4 N O N -C N S A N O M A L Y
1 M IC R O C E P H A L Y , 7 P R E N A T A L R IS K
1 7 C H IL D R E N
"P U R E " A S P H Y X IA L D A M A G E
< 1 0 % O F A L L C P
1 P E R 2 ,7 0 0 B IR T H S
4 0 C H IL D R E N
W IT H A N Y A S P H Y X IA IN D IC A T O R
1 4 9 C H IL D R E N
W IT H N O A S P H Y X IA IN D IC A T O R
1 8 9 C H IL D R E N
W IT H C P
4 5 , 4 4 9
C H IL D R E N

12. All four criteria must be met:
Evidence of metabolic acidosis: umbilical artery pH<7 and base
deficit ≥12 mmol/L at delivery
Early onset of severe or moderate neonatal encephalopathy in
infants ≥34 weeks of gestation
Cerebral palsy of the spastic quadriplegic or dyskinetic type
Exclusion of other identifiable etiologies (eg, trauma, coagulation
disorders, infection, genetic disorders)
Task force on neonatal encephalopathy and cerebral palsy criteria for
Adapted from: Neonatal Encephalopathy and Cerebral Palsy: Executive Summ

13. A sentinel hypoxic event occurring immediately before or during
labor
A sudden and sustained fetal bradycardia or absence of fetal
heart rate variability in the presence of persistent late or
variable decelerations. This usually occurs after a hypoxic
sentinel event with a normal fetal heart rate pattern prior to the
event.
Apgar score of 0 to 5 after five minutes
Onset of multisystem involvement within 72 hours of birth
Early imaging studies showing evidence of an acute nonfocal
cerebral abnormality
Peripartum events that may be related to development of
cerebral palsy but which are not specifically asphyxial
insults
Adapted from: Neonatal Encephalopathy and Cerebral Palsy: Executive Summary. Obstet Gynecol 2004; 103:780.

14. Table 1
Mimics of cerebral palsy
disorder Clue
Familial spastic paraplegia Family history
Transient toe walking Normal deep
tendon reflexes
Muscular dystrophy Calf hypertrophy,
positive Gower’s
sign
Metabolic disorders Regression,
lethargy,
unusual vomiting
Sjogren-Larrson Ichthyosis
Lesch-Nyhan Severe self-
mutilation
Mitochondrial disorders Recurrent stroke,
cardiomyopathy,

15. Impaired movements
• 65% speech defects
• 50% are mentally retarded
• 50% ocular defects
• 25% hearing impairment
• 40% seizure disorders
• 20% seriously disabled
• 1.5 to 2.5 per 1,000 births
will result in severe to
moderately severe

16. Static Vs slowly progressive neurological disorder
Global devlopmental delay/ differential devlopmental
delay

17. Disorder Gross motor Fine motor Social language
Mental
retardation
Delay + + to + + + ++ t+++ +++
Cerebral palsy Delay +++ ++ + +
CP with MR +++ +++ +++ +++
Hearing
impairment
No No No +++
Impaired
vision
++ +
Spinal
muscular
atrophy
++ + + to ++ No Expressive
may be
delayed

18. Levine ( poster) criteria
P- Posturing/ abnormal movement
O- oropharyngeal problems (normality
tongue thrust and swallowing abnormality
S- strabismus
T – tone ( hyper to hypo)
E- Evolutional maldevlopment ( persistent primitive
reflexex or protective / equilibrium reflexes fail to
devlop ( parachute reflex)
R – reflexes ( increased deep tendon/ persistent
babinski

19. Difficulty to diagnose CP during
the 1st
year of life
1. Hypotonia more common then hypertonia in 1st
yr
2. early abundance of primitive reflexes may confuse
3. limited variety of volitional movement for
evolution
4 subtantioal myelination takes months to evovle
5 most instace of CP doesn’t have substancial risk fac

20. What behaviour symptoms
during 1st
year arouse suspicion
of CP
1. excessive irritablity, crying , sleep difficulties
2. early feeding difficulties ( Co-ordination of sucking
and swallowing)
3. Jitter or jerky behavoiur
4. easily startle behaviour
5. Stiffness during dressing , diaper, hand washimg
6. paradoxical precocious devlopment
 a , early rolling ( actually sudden reflex roll rathe
then volitional
Stiff leg standing

21. Feature suggestive of
progressive rather then CP
1. Abnorma increase in heaad circumference
Eye abnormalities
Skin abnormalty
Hepatomegaly and / or spleenomegaly
Decrease or absent deep tendon reflex
Sensory abnormalities
Devlopmental regression ( Rett syndrome )

22. Head and Neck Findings
• 24% inability to chew
• 20% inability to swallow easily
• 20% frequent dental caries
• High rate of temporo-mandibular
disorders

23. Positive signs of spastic CP include:
Spastic hypertonia
Hyperreflexia caused by
hyperexcitability of the stretch reflex
Extensor plantar responses
Clonus

24. Negative signs of spastic CP include:
Slow effortful voluntary movements
Impaired fine-motor function
Difficulty in isolating individual
movements
Fatiguability

25. Athetoid CP Findings (con’t)
• Grimacing
• Drooling
• Speech defects
• Continuous mouth breathers
• Excessive head movements
• Tongue protrusion
• Primitive reflexes of varying severity

26. ASSOCIATED DISORDERS
Intellectual disability
Children with spastic quadriplegia are typically the most severely
affected, while cognitive function usually is better with dyskinetic
CP that is mainly athetoid
Psychiatric disorders
including emotional lability, poor attention and vigilance, and
obsessive-compulsive traits
Epilepsy
most common in patients with spastic quadriplegia and
acquired hemiplegia, and less common in mild symmetric
spastic diplegia and CP that is mainly athetoid

27. Visual disorders
strabismus and clinically significant refractive errors each
occurred in 50 percent, and amblyopia and visual field defects
each
Speech impairment
including aphasia and dysarthria, occur in about 38 percent of
children with CP
Hearing impairment
most common in those with very low birthweight or severe
hypoxic-ischemic insults
Pulmonary disease
a leading cause of death among patients with severe CP
Growth failure Urinary disorders Orthopedic disorders
Osteopenia

28. DIAGNOSIS
The diagnosis of CP depends upon a combination of findings, including motor delay,
neurologic signs, persistence of primitive reflexes, and abnormal postural reactions
Neurobehavioral signs
Motor abnormalities
Developmental reflexes
Laboratory studies
serum concentrations of glucose, thyroid, ammonia, lactate and pyruvate, plasma
amino acid analysis, urine organic acid analysis, and arterial acid-base status,
should be obtained to exclude a metabolic disorder

29. NEUROIMAGING FOR CP
[Bax et al JAMA 2006;296:1602]
Emerging imaging modalities will likely provide further insight
into the etiology of CP by making imaging easier in children
(PROPELLAR) and by mapping white matter tracts (DTI).
The American Academy of
Neurology now recommends
that all cases of cerebral palsy of
unknown origin undergo
neuroimaging
Most children with cerebral palsy
have abnormal neuroradiological
findings, white matter damage
being the most common.

30. lgorithm for the evaluation of the child with cerebral palsy (CP)

31. Cerebral palsy
Clinical Assessment
Goals of Physical Examination
Determine grades of muscle strength and selective
control.
Evaluate muscle tone and determine type.
Evaluate degree of deformity / contracture at each
joint.
Assess linear, angular and torsional deformities of
spine, long bones, hands and feet.
Appraise balance, equilibrium and standing / walking
posture.

32. Cerebral palsy
Goals of Management
(Treatment)
Turn focus of parents from the disease to the goal-
oriented approach
needs time and a lot of
discussion
Physician and Physiotherapist must have the same
perspective

33. Cerebral palsy
Types of Management
(Treatment)
Physical therapy
Orthotics
Control of spasticity
Orthopedic surgery

34. Cerebral palsy
Spasticity
Approaches :
Selective dorsal rhizotomy
Intrathecal baclofen
Botulinum-A toxin

35. Cerebral palsy
Selective Dorsal Rhizotomy
Cut 30 – 50 % of abnormal dorsal rootlets L2 - S1
Followed by intensive physiotherapy
Results encouraging
May cause hyperlordosis / hip subluxation
Best for : spastic diplegia, 4-8 yrs, no previous surgery,
no contractures, no extra pyramidal signs
? Not enough alone
Orthopedic procedures obtain similar results

36. Cerebral palsy
Baclofen
GABA agonist – inhibits release of excitatory
neurotransmitter at level of spinal cord
Oral : mixed reports/ side effects/ not selective
Continuous intrathecal – implantable pump
Good results in releasing spasticity, and improving
function
Complications of pump and catheter
Needs specialized centers

37. Cerebral palsy
Botulinum-A toxin
Acts at myo-neural junctions
Inhibits exocytosis of Acetylcholine
Inject selected muscles at multiple sites
Spasticity reduction may last up to 6 months
Reversible , painless , minimal side effects
Most patients still require lengthening for
permanent correction
Role : - Facilitates physiotherapy and
mobilization
- Delays surgical management
- Trial to determine effects of specific
proposed surgical treatment

38. Cerebral palsy
Physical Therapy
Involve parents as much as possible
(even if they resist)
Do not raise false hopes
which could increase frustration

39. Cerebral palsy
Physical Therapy
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 Orthop.)

40. Cerebral palsy
Orthotics
Immobilization may cause atrophy
Night splints :
- Do not prevent nor reduce deformity
- may cause irritation, pain or stimulate reflexes in
spastic muscles and relaxes the weaker apponents –
thus may increase deformity rather than reduce it !
May be useful only in Athetoid

41. Cerebral palsy
Prerequisites foreffective
surgery
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

42. Cerebral palsy
Prerequisites foreffective
surgery
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

43. Cerebral palsy
Timing For Orthop Surgery
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 could 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

44. The ‘‘Birthday Syndrome’’
One group of complications related to a
chain of operations over the years is social
isolation, loss of motivation, frustration, and
psychosocial problems termed the birthday
syndrome.31

45. SEMLARASS
Single Event Multilevel Lever Arm Restoration Anti
Spasticity surgery

46.  Thanks