CP is a permanent disorder of movement and posture 

- non-progressive 

- brain injury before the age of two years


Strict definition excludes familial & progressive congenital problems & those acquired in childhood as a result of head injuries




2-3 per 1000 live births


Higher in 

- premature and low birth weight children

- low socio-economic group have higher incidence

- more common in advanced countries

(possible increase due to improved survival of premature and low birth weight infants)


Quadriplegia has diminished


Athetosis has been the most dramatic decrease due to

- Rh immunisation

- the drop in erythroblastosis fetalis

- better treatment of jaundiced infants


Most common

- spastic diplegia or hemiplegia

- 65%


Natural History


About 50% have normal intelligence

- 25% end up independent as adults



- hemiplegics 100% walk

- diplegics 75% walk

- quadriplegics 25% walk 


Likely to walk

- sit by 2 years 

- stand by 4 years




Prenatal (44%)


Maternal infection (TORCHS)

- Toxoplasmosis

- Rubella

- Cytomegalovirus

- Herpes

- Syphilis


Maternal exposure

- Alcohol

- Drugs


Perinatal (27%)


Hypoxia (accounts for <10% of CP)


Low birth weight


Postnatal (5%)



Head injury



Other (24%)


Common Causes


Hemiplegia - obstetric

Diplegic - prematurity

Quadriplegia - anoxia

Athetoid - kernicterus


Prematurity Risk


2500 gms = 0.34% 

1500 gms = 14%

<1500 gms = 90%




The lesion that is seen in common is "Periventricular Leukomalacia "




Anatomic and Pathophysiologic classification


It takes at least 2 years to reach a static state


Pathophysiology Classification


Spastic (60%) 

- hyperactive reflexes

- develops contractures, bony deformity & ultimately joint dislocation 

- benefits from orthotics and surgery


Athetoid (10 - 20%)  

- major problems with control of limb position and limb balance

- succession of slow writhing movements

- rarely benefit from orthotics & surgery

- benefit greatly from therapists in terms of self care & occupation programs


Hypotonia (2-5%)

- common in infancy

- most become hypertonic with time


Ataxic (2-5%)

- uncoordinated, unbalanced, wide based gait



- important to identify these children as the motion disorder affects the outcome of surgery

- typically spasticity & athetosis with total body involvement


Spastic - motor cortex

Athetoid - basal ganglia

Ataxic - cerebellar





(True monoplegia or triplegia probably don't occur)



- lower limbs affected much more than upper limbs

- 75% eventually walk

- IQ may be normal

- strabismus is common



- extensive involvement

- low IQ, high mortality

- only 25% able to walk



- usually with spasticity

- develop early handedness

- 100% walk regardless of treatment


Mercer Rang's Stages of CP


Stage 1:  Dynamic contracture

- secondary to spasticity

- physiotherapy / orthotics / botox


Stage 2:  Fixed musculotendinous contractures

- tendon lengthening / transfer


Stage 3:  Bone & joint involvement

- osteotomy / arthrodesis + tendon lengthening




1.  Weakness   


UMN lesion / loss of voluntary movement


2.  Spasticity


Feature of all pyramidal lesions

- excessive activity of disinhibited neurones / overactive stretch reflex

- hypertonicity with increased DTR

- clonus


3.  Contracture


Shortening of the muscle-tendon unit due to failure to keep pace with bony growth

- normally muscles lengthen as bone grows

- as bone grows this worsens spasticity and shortens muscle

- as the muscles don't lengthen get contractures


The sarcomeres add to the muscle at the musculotendinous junction in response to stretch


4.  Deformity


Secondary to unopposed muscle contracture

- worse in all cases where muscles cross 2 joints

- psoas, RF, hamstrings, T Achilles


Hip dislocation

- persistent adduction leads to valgus neck

- persistent flexion leads to anteverted neck

- acetabular dysplasia (deficient posteriorly), hip subluxation and dislocation can follow


It is actually uncertain how increased / decreased tibial torsion and increased femoral anteversion appear




CNS lesion 

Abnormal neurological activity 


Reduced muscle excursion and growth 


Joint instability 

Subluxation / Dislocation 

Degenerative arthritis 


Clinical Features


Spastic Quadriplegia


Usually due to cerebral anoxia



- floppy child that won't feed

- choking during feeds - bulbar palsy

- failure to thrive


The primitive reflexes (Babinski, Moro, Parachute) are preserved


Intelligence / vision / hearing affected

- usually mentally impaired

- may have epilepsy


Only 10-20% will walk 

- can be delayed up to 7 years

- hip dislocation and scoliosis will develop in non ambulators


Spastic Diplegia


Usually due to prematurity


Lower limb affected more than upper

- all milestones delayed

- most walk by 4 years of age


Can vary from mild toe walker to non-ambulators 


Try to improve efficiency of gait 


Spastic Hemiplegia


Usually due to obstetric complications


Usually noticed at walking age

- don't swing one arm

- limp with one - handedness


Right-sided form may have speech delay


Seizures common


All walk independently 

- aim to improve walking appearance or posture of upper limb 




Gross motor function classification system


I  Essentially normal, decreased speed and balance

- walk stairs without aids

- some difficulty on uneven ground


II Hand rail up stairs


III Walker inside, wheelchair outside


IV Wheelchair inside and out


V Nil head support


Orthopaedic Management




1.  ADL's


Upper limb / spine


2.  Mobility


Walking / transferring

- keeping a GMFCS III walking is crucial 

- keeps them out of nursing Home



- 25% TBI (Total body involvement)

- 100% hemiplegics

- 75% diplegics


Prognostic signs

- > 2 primitive reflexes over 1 year poor sign

- should sit at 2 years, walk at 4 years

- TBI v hemi v diplegic




Expert field


Should never decide on treatment at one visit 

- variable nature


Gait analysis lab 

- can help decide best options 


Single Event Multi Level surgery (SEML)

- avoid birthday syndrome (where children are operated on every year)

- has a psychological impact


Surgery between 4-8 years 

- after 8 years tend to develop fixed deformity


Non-operative Management




No scientific evidence that it alters the outcome

- very important nontheless

- high contact with parents  / children

- keeps joints as supple as possible


Cast correction


Young and mild cases




Useful particularly in the equinus ankle where it can be maintained plantigrade in AFO




Botulinium toxin Type A

- blocks acetylcholine release at NMJ

- 50-60% patients respond well 

- for dynamic deformity UL or LL (R1 v R2)



- every 6/12

- peaks at 4/52

- lasts 3-4/12

- at MT junction

- are maps of injection for every muscle in body



- useful in T Achilles

- useful in hamstrings

- overused in psoas

- very useful in UL



A.  Will only fix dynamic spasticity not fixed contracture of muscle

B.  Expense - $500 per IU




R1 v R2

- R1 is passive range of motion performed slowly

- R2 is passive range of motion performed quickly

- a difference between the two indicates dynamic component




Potentiates GABA


Intrathecal Baclofen


GABA analogue




Gilmartin J Paed Neurology 2000

- significant improvement over placebo 

- indicated for spastic quads / TBI

- pump under abdo wall with reservoir

- into spinal cord


Selective Dorsal Rhizotomy 


Best for Spastic Diplegia < 9 without contractures

- need strong legs (as lose some strength with loss of spasticity)

- able to cooperate in rehab

- UL improvement also





- stimulate rootlets to find which mediate spinal reflex

- if only these cut, sensation unchanged

- 30% of dorsal rootlets cut

- decreases feedback from stretch receptors




Spinal deformity

Weakness / parasthesia / bladder problems


Operative Management




1.  Inability to control spastic deformity by non operative measures


2.  Fixed deformity that interferes with function


3.  Joint instability




Stage 1

- physio to help prevent contractures

- botulinum

- splints

- selective posterior rhizotomy


Stage 2 

- tight muscles released / lengthened

- weak muscles augmented by tendon transfers


Stage 3 

- fixed deformities corrected by osteotomy / arthrodesis