CEREBRAL PALSY

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 disease.
Spastic: Upper motor neuron lesion.

Hemiplegia: UMNL of one side of body.

Diplegia: UMNL of all four limbs
but legs more
than arms. May be
symmetric or
asymmetric.
Quadriplegia: Equal involvement of arms
and legs.
Rigidity: increased tone throughout range of movement.
Dyskinesia: Involuntary movements and changes in
muscle tone. Damage to basal ganglia and
extrapyramidal pathways.
Athetosis: Slow writhing movements of limbs.
Extension and fanning of fingers and
extension of wrist.
Chorea: Quick jerky movements of trunk and
proximal limb muscles.
Paraplegia: Legs involved only.
Double Hemiplegia: Bilateral UMNL. Arms and
legs. Also pseudo bulbar
palsy.

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
Diplegia
Quadriplegia
Ataxic

Dyskinetic Dystonic Hypokinesia

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

2. Autosomal recessive.
CEREBRAL PALSY
1. Hemiplegia.
2. Double Hemiplegia.
3. Diplegia (hypotonic, dystonic, spasticity, ataxic).
4. Ataxia.
5. Dysequilibrium Syndrome.
6. Dyskinetic.
7. Mixed.
 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.
PLACENTA
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 thrombosis.
THROMBOPHILIA & CEREBRAL PALSY
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.
 ANTENATAL
Maternal infection & cerebral palsy

a) Maternal fever> 38oc + 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. Breech delivery.
 Cerebral Palsy Associated Disabilities
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
3. Orthopaedic.
4. Speech and Occupational Therapy.
5. Medical.
6. Psychiatric.
Management of Spasticity in Cerebral
Palsy
1. Oral Medicines: Baclofen
Diazepam
Tizanidine
Dantrolene
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.
Prevention
1. Antenatal and Neonatal care.
2. Early detection and advice.
3. Drugs.
4. Immunization and screening.
5. Genetic counselling.
6. Health education.