This document provides information on cerebral palsy, including its definition, causes, classifications, clinical features, complications, investigations, management, and rehabilitation. Cerebral palsy is defined as a static encephalopathy caused by an insult to the developing brain before age 2 that results in motor and/or posture handicaps. It is classified based on etiology, topography, physiology, and functional ability. Spastic cerebral palsy is the most common type. Management involves a multidisciplinary rehabilitation approach including medications, nutrition, physical, occupational, speech, and dental therapies, and surgery if needed. The goals of rehabilitation are to improve functions, develop compensatory abilities, and maximize independence.

1. Cerebral Palsy

2. Definition:
Static Encephalopathy of motor & / or
posture due to an insult to the developing
brain in the 1st two years of life. It consist of
motor handicap & non-motor handicap.

3. Cerebral Palsy
• Key findings in history and physical examination
– History:
• Prematurity
• Light-for-date
• APGAR score
• Blood group incompatibility
• Jaundice
• Respirator or oxygen needed at birth
• The child favors one hand
• A history of neurological infection
• The child has had a seizure
• Any other major illness during the first month of life

4. Cerebral Palsy
• Key Findings Continued:
– Examination
• Persistent automatisms
• Spasticity (Increased muscle tone, hyperactive
reflexes, Babinski response)
• Hypotonia (during the first year of life only)
• Asymmetry of limb development, especially nails
• Disordered movement
• Congenital abnormalities
• Strabismus
• Changes to normal head growth
• Delayed developmental milestones

5. What causes Cerebral Palsy?
• Illness during pregnancy
• Premature delivery
• Accidents such as falling, car crash
• Lead poisoning
• Viral infections
• Lack of oxygen or blood reaching the
newborns brain

6. Causes & Incidence
• Radiation exposure, infection, or use of certain
drugs during 1st 3 months of pregnancy, or
chromosome abnormalities.
• Damage in later stages of pregnancy.
• Birth complications.
• Neo-natal complications
• Incidence is approximately 1 in 500 with the
incidence of boys being affected 30% higher
than girls

7. characteristic features of the disease:
b. Non-motor handicap (≥ 1).
65% speech defect.
50% mental retardation (spastic quariplegia)
50% ocular defect (squint, nystagmus,
refractive error)
40% epilepsy (spastic hemiplegia)
25% hearing defect..
20% frequent dental caries
20% inability to chew.
20% inability to swallow easily.

8. Other associated abnormalities:
• Malocclusion.
• Enamel defect
• GER.
• Drooling of saliva (defective swallowing).
• Constipation.
• Incontinence.
• Recurrent infection.
• Failure to thrive.
The non - motor handicap may be more
important than the motor ones.

9. Prevalence of cerebral palsy:
● 3/1000 to 9/10,000 new babies each year
● During past 3 decades considerable
advances made in obstetric & neonatal
care does not changes prevelance of CP

10. Classification:
A. Etiological.
B. Topographical.
C. Physiological.
D. Functional .

11. Classification:
A. Etiological:
i) Prenatal
ii) Natal
iii) Postnatal
B. Topographical:
i. Monoplegic.
ii. Paraplegic.
iii. Triplegic.
iv. Quadriplegic
v. Diplegic.
vi. Hemiplegic.
vii. Double hemiplegic.

12. C. Physiological:
i. Spastic CP.
ii. Dyskinetic CP.
iii. Ataxic CP.
iv. Atonic CP.
v. Rigid CP
D. Functional:
i. Class I: no limitation to physical activity.
ii. Class II: mild limitation to physical activity.
iii. Class III: moderate limitation to activity.
iv. Class IV: sever (no useful physical activity).

13. A. Etiological classification:
● Most cases = unknown etiology.
● Improvement in perinatal care has little
impact on incidence of CP.

14. ● Prenatal causes… 70%
● Natal causes……..10%
● Postnatal causes…20%

15. Prenatal causes:
• Metabolic (sever hypoglycemia).
• Intrauterine infections – TORCH.
• Brain malformations and infaction.
• Toxins (teratogens drugs - radiation).
• Chromosomal abnormalities.
• Genetic syndromes.
• Rhesus incompatibility.
• Maternal diseases during pregnancy.

16. Natal causes:
• Infection (CNS).
• Asphyxia.
• Prematurity.
Postnatal causes:
• Meningitis.
• Traumatic brain injury.
• Toxins (drugs).

17. ● Risk factors for CP:
– Consanguinity.
– Mother with long menstrual cycle.
– History of spontaneous abortion/stillbirth.
– Family history of CP.
– Malpresentation.
– Low socioeconomic status.

18. B. Topographical classification:
● Monoplegic.
● Paraplegic.
● Triplegic.
● Quadriplegic
● Diplegic.
● Hemiplegic.
● Double hemiplegic.

19. C. Physiological classification:
● Spastic CP……..70%.
● Athetoid CP……65%.
● Ataxic CP………….5%.
● Other rare types……….5%.
- Rigid.
- Flaccid (Hypotonic.)
- Dyskinetic.
- Mixed.

20. ● Spastic CP…. 70%
 Most common type.
 Pathology : ….pyramidal tract.
 Spastic tone (clasp knife) + increased DTR.
• Speech impairment
• Swallowing impairment/drooling
• Spastic tongue.
• Primitive reflexes
 According to limb affected:
- spastic quadriplegia (27%).
- spastic diplegia ( 21%).
- spastic hemiplegia (21%).
- spastic paraplegia.
- spastic monoplegia, triplegia, double
hemiplegia.

21. Spasticity is the commonest affection
of the involved limb.
1. Spastic quadriplegia :
all 4 limbs are equally involved.
2. Spastic diplegia :
all 4 limbs affected with lower more
involved
3. Spastic double hemiplegia:
all 4 limbs affected with upper more
involved.
4. Spastic hemiplegia:
one side of affected with upper more involved.

22. 1. Spastic quadriplegia (27% - CP):
● Most severe form of CP.
● IQ: severe Mental retardation.
● Seizures very frequent.
● Pathology : cystic cavitations of central white
matter of brain.
● Clinical feature:
i) Severe spasticity of all 4 limbs+signs of UMNL
i) Flexion contracture of knee and elbow
( characteristic).
iii) Associated disabillities - speech, vision and
swallowing disorders, athetosis

23. 2. Spastic hemiplegia (21%-CP):
● 25% are mentally retarded.
● 30% have seizure by 2nd year.
● Aetiology : intrauterine thromboembolism
● Pathology: revealed by CT-scan/MRI :
– Atrophy of cerebral hemisphere on contra lateral
side.
– Dilation of lateral ventricle on the affected side.

24. Clinical feature:
– One side affected (spastic – weak ).
– Upper limb more affected than lower
– Decreased spontaneous movement on affected
side .
– Delayed walking (18 – 24).
– Abnormal gait (circumduction).
– Dystonic posture of UL in running.
– UL: Adduction at shoulder, flexion at elbow
and wrist joints.
– LL: Abduction at hip, extention at knee and ankle
joints.
– Equinovarus deformity of affected LL.
– Increased DTR. Clonus, +ve babiniski sign.

25. 3. Spastic diplegia (21% -CP):
● IQ : excellent.
● Seizure : less frequent.
● Etiology :common factor is prematurity.
● Pathology: periventricular leukomalacia.

26. Clinical feature:
 Prominant spasticity of LL + signs of UMNL.
 Difficulty in application of diaper (early
symptom).
 Commando crawl.
 Maintained scissoring of LL when suspended
from axilla.
 Walking: delayed, tip toe .
 Disuse atrophy of LL.

27. Athetoid CP:
● IQ: preserved in most patient.
● seizure: uncommon.
● etiology: hyperbilirubinemia (neonatal
period).
● athetosis  main clinical feature.
(athetosis=uncontrollable writhing
movements at distal extremities ).
● involves all four extremities
● Neck and face may be involved
● Voluntary movements are flailing
● Difficulty up righting and balancing

28. Other features:
• Excessive head movements.
• Tongue protrusion.
• Drooling.
• speech defects : (oropharyngeal
muscles).
• Continuous mouth breathers
• Primitive reflexes retention.

29. ● Ataxic CP:
- Broad based gait (unsteady gait with
feet far apart).
- Affects balance and coordination.
- Difficulty with motions requiring
precise coordination such as writing.

30. ● Dyskinetic CP:
- all 4 limbs are affected.
- abnormal movement.
- movement is chorioathetoid or
dystonic.
chorioathetoid movement

33. D. Functional classification:
● class I: no limitation to physical activity.
● class II: mild limitation to physical activity.
● class III: moderate limitation to activity.
● class IV: severe (no useful physical activity).

34. Differential diagnosis of CP:
1. Neurodegenerative disorders:
 Initial normal and subsequent slowing of
milestones.
 Loss of previously attained milestones.
 Unusual body odour.
 +ve family history.
 Hypotonia without hyperreflexia.
 Primary ataxia.
2. spinal cord lesions.
3. myopathy.
4. primary mental retardation.

35. Cerebral Palsy: Complications
• Spasticity
• Weakness
• Increase reflexes
• Clonus
• Seizures
• Articulation &
Swallowing difficulty
• Visual compromise
• Deformation
• Hip dislocation
• Kyphoscoliosis
• Constipation
• Urinary tract infection

36. important points in history:
- Pregnancy: prematurity, maternal diseases
(uncontrolled diabetes, maternal
hypertention)
- Delivery: emergency C/S.
syntocinon – 1st stage of labour.
prolonged rupture of menmbrane.
prolonged 2nd stage of labour.
- After birth: prematurity signs/ small size baby
delayed weak cry, delayed poor suckling,
hyperbilirubinrmia, neonatal seizers, RDS

37. Investigations:
● Diagnosis is mainly clinical.
● Investigations  for underling pathology
e.g : CT, MRI of brain.
or when other differential is possible.
● Relevant investigations include:
a. TORCH screen.
b. Urine for metabolic screening.
c. Chromosomal analysis.

38. Management of CP
Goals of management:
1. improve preserved functions.
2. develop compensatory functions.
3. encourage independence.
4. maintain normal growth.
5. facilitate communocation.
6. insure good dental hygiene
------------------- REHABILITATION

39. Why Rehabilitation?
What is the chance to
have:
normal IQ. - 50%.
normal speech - 35%
normal hearing - 75%

40. REHABILITATION:
● Team management:
o Pediatric neurologist.
o Physiotherapiest.
o Occupational therapist.
o Orthopedic/neuro surgeon.
o Speech therapist.
o Social workers.
o Nutritionist.

41. ● Types of management :
a) Medications:
1. Anticonvulsive
Carbemezapine, Phenytoin,
Phenobarbitone.
2. Antispastic drugs:
Baclofen, Dantrolene, Benzodiazipines.
3. Antireflux drugs:
Metoclopramide, Cisapride.
4. Anticonstipation drugs.
5. Antibiotics (when needed) .

42. b) Nutritional care:
• Regular follow up of weight.
• Gastric tube (home).
• Nasogastric tupe (hospital).
c) Hearing care:
Assessment and treatment of hearing deficit
 Mild deficit: 24 – 45 db loss=no intervention
 Mod. deficit: 45-65 db loss=hearing aids.
 Sever deficit: 65-85 db loss= amplification.
 Profound deficit:>85 db loss= special
education for deaf

43. d) Vision care:
 Use of spectacles.
 Surgical correction of squint.
e) Dental care:
• Evaluate ability to clean
• Highlight importance to parents.
• Modified toothbrush.
• Fluoride
• Non non-carious food.

44. f) Physiotherapy:
 Most important care especially for
spastic CP
 Maintain maximum range of joints
movement to attain at least daily activity
e.g: combing hair, brushing teeth,
bathing, toilet, dressing, driving specially
reformed vehicles.
 >>>>> insure dependency.

45. g) Surgical procedures:
• Contractures
• Spasticity not responding to drugs.
• Deformity
• Severe scoliolsis.
h) Social and economical support :
 Friendship societies, health insurance…etc)