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CEREBRAL PALSY
Introduction 
• Historically known as static encephalopathy 
• A group of motor impairment syndromes 
resulting from disorders of early brain 
development. 
• Often associated with epilepsy and 
abnormalities of speech, vision and intellect. 
• However, many children and adult with CP 
function at a high educational and vocational 
level without sign of cognitive dysfunction
Epidemiology 
• CP is the most common and costly form of 
chronic motor disability 
• Prevalence: 2/1000 
• Prevalence of CP is increased in low birth 
weight infants (<1000g) 
• CP incidence higher in premature and twin 
birth
Aetiology 
Caused by developmental, genetic, metabolic, 
ischemic, infections 
•Infection 
- German measles 
- Shingles 
•Diabetes 
•Toxemia of 
pregnancy 
•Rh incompatibility 
•Asphyxia 
•Birth injury 
•Prematurity 
Antenatal 
factors (80%) 
Intrapartum 
(10%) 
Postpartum 
(10%) 
• Very high fever 
• Brain infection 
• Head injury 
• Lack of oxygen 
• Poisoning 
• Intracranial 
hemorrhage or 
blood clot
Risk Factors 
• Before Pregnancy: 
- History of fetal wastage 
- Long menstrual cycle 
- Maternal thyroid disorder 
- Family history of mental 
retardation 
• During Labor and Delivery: 
- Premature separation of 
placenta 
• During Early Postnatal Period: 
- Newborn hypoxic ischemic or 
bilirubin (kernicterus) 
encephalopathy 
• During Pregnancy: 
- Low socioeconomic status 
- Tx of mother with thyroid 
hormone, estrogen or 
progesterone 
- Maternal seizure disorder 
- Polyhydramnios 
- Eclampsia 
- Bleeding in 3rd trimester 
- Twin gestation 
- Congenital malformation 
- Fetal growth retardation 
- Abnormal fetal presentation
Classification 
Physiologic 
identify forms of motor 
impairment 
Spastic CP 
Dyskinetic CP 
Ataxic CP 
Mixed CP 
Distribution 
identify location of 
musculoskeletal involvement 
Spastic diplegia 
Spastic 
quadriplegia 
Spastic hemiplegia
Spastic CP 
• The most common form of CP 
(70-80%) 
• Due to injury to upper motor 
neurons of pyrimidal tract 
• Often exhibit truncal hypotonia 
in 1st year of life
•Characterized by at least 2 of following: 
-Abnormal movement pattern 
-Increased tone 
-Pathologic reflexes (Babinski, hyperreflexia)
Dyskinetic CP 
• 10-15% 
• Result of injury to basal ganglia (associated 
with kernicterus) 
• Characterized by variable tonal abnormalities 
& involuntary movement (athetosis, chorea) 
• Fewer seizures & >normal cognitive function
Ataxic CP 
• <5% of CP cases – rare 
• Results from cerebellar injury 
• Abnormalities of voluntary movement and 
balance 
• Wide-based, unsteady gait, abnormal muscle 
tone
Mixed CP 
• 10-15% of all cases 
• > 1 type of motor pattern is 
present & when 1 pattern 
does not clearly dominate 
another 
• Associated with > 
complications: sensory 
deficits, seizures, cognitive-perceptual 
impairments
Dystonic CP 
• Uncommon 
• Characterized by reduced activity and stiff 
movement (hypokinesia) and hypotonia
Choreoathetotic CP 
• Rare 
• Caused by excess hyperbilirubinemia 
• Dominated by increased and stormy 
movement (hyperkinesia) and hypotonia
Clinical Manifestations 
• Spectrum of developmental abnormalities 
• Mental retardation 
• Epilepsy 
• Motor handicap
•Visual, hearing, speech, cognitive & 
behavioral abnormalities
Spastic diplegia 
• 25-35% 
• Bilateral spasticity of legs 
• 1st noted when infant begins to crawl 
• Child uses arm normally but drag the legs 
behind 
• Application of diaper is difficult 
• Unable to sit
• On examination: 
- Brisk reflexes 
- Ankle clonus 
- Bilateral Babinski sign 
- Scissoring posture of lower extremities 
• Delayed walking 
• Feet in equinovarus 
• Walk on tiptoe 
• Disuse atrophy
Spastic hemiplegia 
• Decreased spontaneous movements on 
the affected side 
• Show hand preference at very early age 
• Difficulty in hand manipulation 
• Delayed walking 
• Circumductive gait 
• Growth arrest in hand and thumbnails 
• Equinovarus of foot 
• Walks on tiptoe
• Ankle clonus 
• Babinski sign 
• Increase deep tendon reflexes 
• Weakness of hand and foot dorsiflexors 
• 1/3 have seizure, cognitive abnormalities
Spastic quadriplegia 
• The most severe form 
• Marked motor impairment of all 
extremities 
• Mental retardation & seizure 
• Swallowing difficulty
• Increased tone and spastic 
• Decreased spontaneous movement 
• Brisk reflexes 
• Plantar extensor response 
• Flexion contraction of knee and elbow 
• Speech & visual abnormalities 
• Athetosis
Athetoid CP 
• Less common 
• Dyskinetic CP 
• Associated with birth asphyxia 
• Hypotonic with poor head control, head lag
• Increased variable tone with rigidity and 
dystonia 
• Feeding difficulty, tongue thrust, drooling
Diagnosis 
• History and PE should preclude 
progressive disorder of CNS, 
degenerative disease, metabolic 
disorders, spinal cord tumor, 
muscular dystrophy 
• MRI scan of brain or spinal cord 
• Test of hearing and visual function 
• Genetic evaluation
Management 
• CP cannot be cured 
• Family support – educate parents
• Adjunctive therapy: 
- Physiotherapy 
- Occupational therapy 
- Speech therapy 
• Surgery 
• Psychologist or psychiatrist
•Adaptive equipment
• Drugs: 
- Oral dantrolene sodium, benzodiazepines, 
baclofen – treat spasticity 
- Botulinum toxin 
- Levodopa
Thank you!! 
References: 
• Kliegman, Behrman, Jenson & Stanton (2007). Nelson 
Textbook of Pediatrics. 18th Edition 
• Kliegman, Jenson, Marcdante & Berhman (2006). Nelson 
Essentials of Pediatrics. 5th Edition

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Cerebral palsy

  • 2. Introduction • Historically known as static encephalopathy • A group of motor impairment syndromes resulting from disorders of early brain development. • Often associated with epilepsy and abnormalities of speech, vision and intellect. • However, many children and adult with CP function at a high educational and vocational level without sign of cognitive dysfunction
  • 3. Epidemiology • CP is the most common and costly form of chronic motor disability • Prevalence: 2/1000 • Prevalence of CP is increased in low birth weight infants (<1000g) • CP incidence higher in premature and twin birth
  • 4. Aetiology Caused by developmental, genetic, metabolic, ischemic, infections •Infection - German measles - Shingles •Diabetes •Toxemia of pregnancy •Rh incompatibility •Asphyxia •Birth injury •Prematurity Antenatal factors (80%) Intrapartum (10%) Postpartum (10%) • Very high fever • Brain infection • Head injury • Lack of oxygen • Poisoning • Intracranial hemorrhage or blood clot
  • 5. Risk Factors • Before Pregnancy: - History of fetal wastage - Long menstrual cycle - Maternal thyroid disorder - Family history of mental retardation • During Labor and Delivery: - Premature separation of placenta • During Early Postnatal Period: - Newborn hypoxic ischemic or bilirubin (kernicterus) encephalopathy • During Pregnancy: - Low socioeconomic status - Tx of mother with thyroid hormone, estrogen or progesterone - Maternal seizure disorder - Polyhydramnios - Eclampsia - Bleeding in 3rd trimester - Twin gestation - Congenital malformation - Fetal growth retardation - Abnormal fetal presentation
  • 6. Classification Physiologic identify forms of motor impairment Spastic CP Dyskinetic CP Ataxic CP Mixed CP Distribution identify location of musculoskeletal involvement Spastic diplegia Spastic quadriplegia Spastic hemiplegia
  • 7.
  • 8. Spastic CP • The most common form of CP (70-80%) • Due to injury to upper motor neurons of pyrimidal tract • Often exhibit truncal hypotonia in 1st year of life
  • 9. •Characterized by at least 2 of following: -Abnormal movement pattern -Increased tone -Pathologic reflexes (Babinski, hyperreflexia)
  • 10. Dyskinetic CP • 10-15% • Result of injury to basal ganglia (associated with kernicterus) • Characterized by variable tonal abnormalities & involuntary movement (athetosis, chorea) • Fewer seizures & >normal cognitive function
  • 11. Ataxic CP • <5% of CP cases – rare • Results from cerebellar injury • Abnormalities of voluntary movement and balance • Wide-based, unsteady gait, abnormal muscle tone
  • 12. Mixed CP • 10-15% of all cases • > 1 type of motor pattern is present & when 1 pattern does not clearly dominate another • Associated with > complications: sensory deficits, seizures, cognitive-perceptual impairments
  • 13. Dystonic CP • Uncommon • Characterized by reduced activity and stiff movement (hypokinesia) and hypotonia
  • 14. Choreoathetotic CP • Rare • Caused by excess hyperbilirubinemia • Dominated by increased and stormy movement (hyperkinesia) and hypotonia
  • 15. Clinical Manifestations • Spectrum of developmental abnormalities • Mental retardation • Epilepsy • Motor handicap
  • 16. •Visual, hearing, speech, cognitive & behavioral abnormalities
  • 17. Spastic diplegia • 25-35% • Bilateral spasticity of legs • 1st noted when infant begins to crawl • Child uses arm normally but drag the legs behind • Application of diaper is difficult • Unable to sit
  • 18. • On examination: - Brisk reflexes - Ankle clonus - Bilateral Babinski sign - Scissoring posture of lower extremities • Delayed walking • Feet in equinovarus • Walk on tiptoe • Disuse atrophy
  • 19. Spastic hemiplegia • Decreased spontaneous movements on the affected side • Show hand preference at very early age • Difficulty in hand manipulation • Delayed walking • Circumductive gait • Growth arrest in hand and thumbnails • Equinovarus of foot • Walks on tiptoe
  • 20. • Ankle clonus • Babinski sign • Increase deep tendon reflexes • Weakness of hand and foot dorsiflexors • 1/3 have seizure, cognitive abnormalities
  • 21. Spastic quadriplegia • The most severe form • Marked motor impairment of all extremities • Mental retardation & seizure • Swallowing difficulty
  • 22. • Increased tone and spastic • Decreased spontaneous movement • Brisk reflexes • Plantar extensor response • Flexion contraction of knee and elbow • Speech & visual abnormalities • Athetosis
  • 23. Athetoid CP • Less common • Dyskinetic CP • Associated with birth asphyxia • Hypotonic with poor head control, head lag
  • 24. • Increased variable tone with rigidity and dystonia • Feeding difficulty, tongue thrust, drooling
  • 25.
  • 26. Diagnosis • History and PE should preclude progressive disorder of CNS, degenerative disease, metabolic disorders, spinal cord tumor, muscular dystrophy • MRI scan of brain or spinal cord • Test of hearing and visual function • Genetic evaluation
  • 27. Management • CP cannot be cured • Family support – educate parents
  • 28. • Adjunctive therapy: - Physiotherapy - Occupational therapy - Speech therapy • Surgery • Psychologist or psychiatrist
  • 30. • Drugs: - Oral dantrolene sodium, benzodiazepines, baclofen – treat spasticity - Botulinum toxin - Levodopa
  • 31. Thank you!! References: • Kliegman, Behrman, Jenson & Stanton (2007). Nelson Textbook of Pediatrics. 18th Edition • Kliegman, Jenson, Marcdante & Berhman (2006). Nelson Essentials of Pediatrics. 5th Edition