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Chronic disability of central nervous system

origin characterised by aberrant control of
movement of posture, appearing early in life
and not the result of progressive neurological
Spastic: Upper motor neurone lesion.

Hemiplegia: UMNL of one side of body.

Diplegia: UMNL of all four limbs but legs more

than arms. May be symmetric or

Quadriplegia: Equal involvement of arms and legs.

Rigidity: tone throughout range of movement.

Dyskinesia: Involuntary movements and changes in muscle

tone. Damage to basal ganglia and
extraphyomides pathways.

Athetosis: Slow writhing movements of limbs. Extension

and fanning of fingers and extension of wrist.

Chorea: Quick jerky movements of trunk and prox, limb

Paraplegia: Legs involved only.

Double Hemiplegia: Bilateral UMNL. Arms and

legs. Also pseudobulbar

Monoplegia: One Limb.

Cerebral Palsy Rates

Multiple births 7.5 / 1000 live births

Singletons 2.1 / 1000 live births

1500gr or less 80 / 1000

Types of Cerebral Palsy
Spastic Hemiplegia


Dyskinetic Dystonic Hypokinesia

Chored-Athetoid Hyperkinesia
Dysequilibrium Syndrome
1. Difficulty in maintaining an upright
position and in experiencing the position
of the body in space.

2. Autosomal recessive.
1. Hemiplegia.
2. Double Hemiplegia.
3. Diplegia (hypotonic, dystonic,
spasticity, ataxic).
4. Ataxia.
5. Dysequilibrium Syndrome.
6. Dyskinetic.
7. Mixed.
Of 229 children cerebral palsy at 1 year
of age, more than were free of motor
handicap at 7 years.

COLLAB, Perinatal Project

Early Signs of Cerebral Palsy
1. Birth History
a) Prematurity.
b) Seizures.
c) Low apgars.
d) Intracranial haemorrhage.
e) Periventricular leucomalacia.
2. Delayed Milestones
3. Abnormal Motor Performance
a) Handedness.
b) Reptilian crawl.
c) Toe waking.
Early Signs of Cerebral Palsy
4. Altered Tone.

5. Persistence of primitive reflexes.

6. Abnormal posturing.
Prenatal Associations with
Cerebral Palsy

Placental insufficiency.
Brain malformation.
Congenital infection.
Chromosomal defects.
Exposure to toxins.
Abnormality of neuronal migration.
1. Correlation of placenta infarction or
thrombosis with ischaemic lesions in the
brains of babies who have suffered
intrauterine or early neonatal deaths.

2. 11 / 15 placental slices from 15 patients

with Cerebral Palsy contained
a) Thrombosis in placental circulation.
b) Coagulation abnormalities in mother and foetus
Factor V Leiden Mutation which is responsible for
activated protein C resist (APCR).
c) Foetal and neonatal stroke have been reported in
presence of maternal anticardiolipin antibodies.
d) 20 / 31 children with cerebral palsy had one or
more disorders of coagulation in neonatal blood
spot analysis.
Maternal infection & cerebral palsy

a) Maternal fever> 38 c + Chorioamnionitis
associated with risk of cerebral palsy.

b) Inflammatory markers in children with

cerebral palsy.
Cerebral Palsy
1. Fall in incidence of Cerebral Palsy in low birth
weight babies.
2. in incidence in babies 2.5-4kg (2/3 of cases).
3. Excess boys (C58%).
4. in incidence of dyskinetic cerebral palsy.
5. in lowest socio-economic groups.
6. Maternal age and parity.
U shaped curve < 20 years - > 34 years.
4 children or >.
7. Breach delivery.
Cerebral Palsy Associated
Mental retardation 1/3 N. 1/2 I.Q. < 55.
Epilepsy 20-50% > generalised.
Speech disorders 50% delay/dysarthria.
Vision and hearing 25%.
Behaviour abnormalities.
Learning difficulties.
Common Management
Problems in Cerebral Palsy
1. Feeding Problems:
Failure to suck.
Tongue trusting, gagging and choking.
Vomiting and regurgitation.
2. Dribbling.
3. Constipation.
4. Crying, screaming and sleep disturbances.
5. Chilblains and cold injury.
6. Growth.
Treatment of Cerebral Palsy
1. Parent guidance.
2. Physiotherapy - Bobath method.
3. Orthopaedic.
4. Speech and Occupational Therapy.
5. Medical.
6. Psychiatric.
Management of Spasticity in
Cerebral Palsy
1. Oral Medicines: Baclofen
2. Intrathecal Baclofen.
3. Botulinum Toxin.
4. Selective Posterior Rhizotomy.
Botulinum Toxin
1. Produced by bacterium clostridium Botulinum.
2. Blocks release of Acetylcholine from cholinergic
nerve terminals.
3. Duration of effects, 3-4 months.
4. Adverse effects: muscle weakness.
Allergic reaction rare.
Autonomic Dysfunction.
Occasional flu like symptoms.
Antibody development.
1. Antenatal and Neonatal care.
2. Early detection and advice.
3. Drugs.
4. Immunization and screening.
5. Genetic counselling.
6. Health education.