1. CEREBRAL PALSY
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2. DEFINITION
CEREBRAL PALSY (CP) is also known as LITTLE’S DISEASE or STATIC ENCEPHALOPATHY.
It is defined as a disorder of posture and movement which is caused by a permanent and non-progressive insult to the developing brain.
The permanent brain lesion that results in CP affects other brain functions apart from the motor area resulting in speech, auditory, visual and mental deficits but these are NOT part of the definition of CP.
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3. CP results from an abnormality in or injury to the cerebrum — the largest area of the brain, which controls sensation and voluntary motor function.
Although CP affects movement, the underlying problem originates in the brain, not in the muscles themselves.
The cerebral lesion is STATIC but the movement disorder may change with time.
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4. EPIDEMIOLOGY
The Collaborative Perinatal Project in US, in which approximately 45,000 children were regularly monitored from pregnancy to the age of 7yr, reported the prevalence of CP to be 4/1,000 live births.
The prevalence of Cerebral Palsy among children attending Paediatric Neurology Clinic in OOUTH between 1996 and 2000 was 50.3%
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5. AETIOLOGIES
These vary in different parts of the world depending on the spectrum of prenatal, perinatal or postnatal insults to which the fetal and neonatal brains are exposed.
Intra-uterine infections and extreme prematurity are the commonest causes of CP in the developed world, perinatal hypoxia arising from poor neonatal resuscitation at birth is the most common cause in the developing world.
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6. AETIOLOGIES PRENATAL Intra-uterine infections (TORCHES)
Intra-uterine hypoxia
Antepartum haemorrhage
Congenital cerebral malformations
Irradiation
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7. AETIOLOGIES PERINATAL Prematurity Asphyxia (Commonest in OOUTH)
Cord prolapse
Intracranial haemorrhage
Hypoglycaemia
Kernicterus (2nd leading cause in OOUTH)
Neonatal convulsions (apart from hypocalcaemia)
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8. AETIOLOGIES POSTNATAL Meningitis Encephalitis
Head trauma with intracranial bleeding
Prolonged seizures (of any aetiology)
Hypertonic dehydration
Lead toxicity
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9. PATHOLOGY CORTICAL ATROPHY Neuronal loss Gliosis Microcephaly
Widened ventricles
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10. CLINICAL FEATURES Cardinal features of CP include:
Delay in motor developmental milestones
Abnormalities of muscle tone
Reduction in normal movement
Presence of abnormal movements
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11. TYPES OF CEREBRAL PALSY
SPASTIC – upper motor neurone pattern of weakness, hypertonia, hyper-reflexia & extensor plantar reflex. May be lead-pipe or clasp-knife in form. Most common type – about 75% of cases.
Hemiplegia (one side; upper limb more affected than lower limb)
Diplegia (both lower limbs more affected than upper limbs; associated with prematurity)
Quadriplegia (all limbs equally affected) *****
Double hemiplegia
Paraplegia (very rare)
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12. TYPES OF CEREBRAL PALSY
ATHETOID (DYSKINETIC) –continuous, slow, writhing movements, due to basal ganglia damage from either kernicterus or asphyxia. Usually associated with auditory and speech defects but intellect is often preserved. About 20% of cases.
ATAXIC (EXTRAPYRAMIDAL) - lack of balance reactions, intention tremors, broad based gait, in-coordination of hand movements. Associated with prenatal cerebellar damage. Least common type.
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13. TYPES OF CEREBRAL PALSY
HYPOTONIC- Hypotonia is present at rest but features of UMNL may manifest. Usually severely mentally retarded. Uncommon.
MIXED - a combination of different types.
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14. FUNCTIONAL CLASSIFICATION
CLASS I – no limitation of activity
CLASS II – slight to moderate limitation
CLASS III – moderate to severe limitation
CLASS IV – no useful physical activity
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15. CLUES TO EARLY DIAGNOSIS
Delayed motor milestones
Apathy
Floppiness
Stiffness
Scissoring
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16. CLUES TO EARLY DIAGNOSIS
Persistent fisting
Violent startle reactions
Sialorrhoea
Paucity of movements
Strong hand preference in the first year of life
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17. ASSOCIATED PROBLEMS Mental retardation (occurs in ≈ 66% of cases)
Seizure disorders
Deafness
Blindness, squints, refractive disorders
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18. ASSOCIATED PROBLEMS
Orthopaedic problems (hip dislocation, contractures like toe-walking and scoliosis)
Behavioural disorders (incontinence, constipation etc)
Sialorrhoea
Attention Deficit & Hyperactivity Disorder
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19. DIAGNOSIS Thorough history (prenatal, perinatal & postnatal)
Physical examination (motor system & sensory organs)
CT scan or MRI of the brain
Baseline EEG
Audiometry
Ophthalmologic evaluation
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20. DIFFERENTIAL DIAGNOSIS
Neurodegenerative diseases
Sphingolipidosis
Glycogen storage diseases
Adrenoleukodystrophies
Spinal cord tumours
Muscular dystrophies
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21. MANAGEMENT Early diagnosis and institution of treatment is desired.
Requires multi-disciplinary approach (paediatric neurologist, paediatric nurse, physiotherapist, speech therapist, orthopaedic surgeon, social worker, educator).
Parents should be taught to address the peculiarities of daily activities such as feeding, dressing, bathing and playing in ways that limit the effects of abnormal muscle tone.
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22. MANAGEMENT
Use of adaptive equipments like walkers, poles, and standing frames, motorized wheelchairs, special feeding devices and customized seating arrangements.
Drugs (Dantrolene sodium 0.5mg/kg/ dose bd; Baclofen 10-15mg/day, Diazepam mg/kg/dose bd) to reduce spasticity.
Direct injection of Botulinum toxin into the affected muscle is still undergoing trials.
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23. MANAGEMENT Hearing and vision aids Orthotics like braces and splints
Enrolment in special schools
Communication skills may be enhanced by the use of special devices.
Surgical procedures like release of contractures and dorsal rhizotomy (transection of dorsal nerve roots supplying spastic muscles).
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24. PREVENTION Prevent birth asphyxia
Early diagnosis and prompt intervention in neonatal jaundice.
Prevent intra-uterine infections with immunization with MMR
NICU for extremely premature infants has been shown to increase the survival of these vulnerable babies & the incidence of CP.
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