This document discusses cerebral palsy (CP), defining it as a group of non-progressive movement disorders caused by brain insults during development. It covers the etiology, pathology, clinical features and classifications of CP. Etiology includes congenital, acquired, and infective causes. Pathology includes subependymal hemorrhage, periventricular leukomalacia, and hypoxic-ischemic damage. Clinical features include motor control disorders along with cognitive, sensory, and behavioral symptoms. Diagnosis involves developmental screening and clinical exams. Management is multidisciplinary, including therapies, medications, and sometimes surgery. Prevention focuses on good antenatal and neonatal care.

1. DR.G.ANANTHA REDDY
MD.DM, DCH
NEUROLOGIST
RETD.PROFESSOR OF PEDIATRICS.

2. 1.INTRODUCTION
2.DEFINATION
3.ETIOLOGY CLASSIFICATION
4.PATHOLOGY CLASSIFICATION
5.CLINICAL FEATURES CLASSIFICATION
6.DIAGNOSIS
7.MANAGEMENT
8.PREVENTION

3. 1.INTRODUCTION
 a. 1862 JHON HITLER DISCOVERED
 b. FREUD COIND TERMINOLOGY
 c. WHAT IS CEREBRAL PALSY
 d. WHAT IS NOT CEREBARL PALSY
 e. HOW BIG IS THE PROBLEM OF CEREBRAL PALSY
1.2 to 2.5 per 1000 school age children
Incidence 2 per 1000 live births.
25 lacks in India
7 lacks in USA.

4. DEFINATION
CP does not refer to a single entity but is a group of
non progressive disorders of heterogenous etiologies
that manifest as abnormalities of movement of posture
resulting from insult to developing C.N.S which occur
during prenatal, natal, post natal period till one
month of age.

5. ETIOLOGY
 THREE BROAD GROUPS
 1. CONGENITAL CAUSES OF CEREBRA PALSY.
 2. ACQUIRED CAUSES OF CEREBRAL PALSY.
10 TO 18 % OF CEREBRAL PALSY
 3. INFECTIVE CAUSES OF CEREBRAL PALSY

6. 1.CONGENITAL CAUSES OF CEREBRAL PALSY
 a. Prematurity.
 b. L.B.N
 c. Small for her gestational age
 d. Intrauterine hypoxia and prenatal hypoxia
 e. Maternal malnutrition
 f. Placental infarction
 g. Congenital malformations
 h. Bilirubin encephalopathy and hypoglycemia
 i. Genetic and chromosomal
 J. Environmental factors

7. AQUIRED CAUSES OF CEREBRAL PALSY
 Septicemia
 Meningitis
 Encephalitis
 Head trauma
 Neonatal seizures
 Extreme hypoglycemia
 Kernicterus

8. INFECTIVE CAUSES OF CEREBRAL PALSY
 TORCH infections previously
 LATCH
 Listeria Monocytogenes
 AIDS; HIV
 Toxoplasmosis
 Cytomegalo infections
 Herpes simplex infection

9. PATHOLOGY CLASSIFICATION
 A. SUB EPENDYMAL HEMORRHAGE
premature 25-35 weeks G.A
L.B.W 1.8 KG or Less.
Lesser degree of hemorrhage – Survive and develop
hydrocephalus.
HAGBERGA - SWEEDISH
Half patients with spastic Diplegia had matrix hemorrhages
P.L.M

10. B. PERIVENTICULAR LEUCOMALACIA
 At water shed zones of cortical and central arteries
represents venous infarcts.
 May develop in premature and full term infants
suffering hypotension and apnea.
 High risk 28 weeks G.A.
 Survivors develop cerebral Hemiplegia or Diplegia &
cognitive impairment.

11. C. HYPOXIC ISCHEMIC DAMAGE-
NEONATAL ENCEPHALOPATHY
 FENICHEL & SARNAT 1976
 Mild, Moderate, Severe HIE
 For moderate & severe HIE
Risk factors are Toxemia, Ante partum
hemorrhage, SGA, preterm.
• Some are term infants develop HIE birth process may
or may not be abnormal
• SIGMOND FREUD THEORY

12. INTERM INFANTS CAUSES OF HIE ARE MAINLY
 a. T.S.G.A
 b. Toxemia of pregnancy
 c. Placental infarction
 d. Intrauterine asphyxia
Results in cerebral Diplegia other spastic, dystonic,
ataxic syndromes.
D. Where a, b, c factors are not operative

13. RECENT STUDY OF COWAN & COLLEAGUES
 MRI in neonatal encephalopathy excluding major
congenital malformations, chromosomal
abnormalities.
 80 % no established lesion or cerebral atrophy in
neonatal encephalopathy.
 But in neonatal seizures 69% antenatal damage.
 Clinical syndromes due to pathology: -
 Matrix, hemorrhage, PVL, HIE, Kernicterus is Spastic
Diplegia.

14.  Hypoxic ischemic injury in term or preterm infants
take form of :
 a. Hemiplegia.
 b. Double Hemiplegia.
 c. spastic ataxic syndromes.
Spastic quadriplegia & MR due to major insuiits like
intrapartum asphyxia & fetal distress.
Pathology is ulegyric sclerotic cortex in white matter of
parietal and posterior frontal lobes.

15.  MAJOR CONTROL & POSITVE DISORDERS
CLASSIFIED AS
 1. Spastic form
 a. Spastic Quadriplegia
 b. Spastic Diplegia
 c. Spastic Hemiplegia.
 2. Hypotonic form.
 3. Ataxic form.
 4. Dyskinetic form.
 a. Choreoathetosis.
 b. dystonic or both.
 5. Mixed form
 Spastic & choreoathetotic form

16. CLINICAL FEATURES & CLASSIFICATION
Mainly motor control disorders with accompanied symptoms.
 1. Cognitive
 2. Sensory visual hearing.
 3. Communication defect.
 4. Growth failure
 5. Seizures
 6. Behavior & emotional problems.
 a. attention deficit.
 b. depression.
 c. dependency.
 d. defective sexuality.
 e. low self esteem.

17. DIAGNOSIS
 Developmental Screening
 H/O High risk infant.
 H/O drug addiction in the mother.
 MR or psychotic illness of mother.
 Disturbed family
 Dynamic
 Clinical Exam:
see development mile stones:
Eyes, Ears, Musculoskeletal survey, Head
circumference.
 Observe early pointers to CP

18. LABORATORY ASSESSMENT & IMAGING
 CT Brain
 MRI Brain
 EEG
 EMG
 Metabolic screening
 Blood – for sugar, calcium, ammonia, lactic acid.
 ABG
 Aminoacidopathy screening
 T3, T4, TSH and finally D.D.S.T clinical psychological
testing.

19. MANAGEMENT MULTIDISCIPLINARY APPROACH
 a. Early intervention
 b. physiotherapy & occupational therapy
 c. special education.
 cognitive therapy.
 behavior therapy.
 Speech therapy.
 Pharmacotherapy.
 seizures - AEDS
 Spasticity - BACLOFEN
1.25 to 2.5 mg b.i.d. > 30mg/day.
Does not improve coordination

20.  1. INTRATHECAL BACLOFEN FOR SEVERE SPASTICITY :
BENODIAZIPINS, DANTROLENE, TIZANIDINE are
tried.
 2. DYSTONIA:
LEVODOPA, CARDAMAZEPINE,
TRIHEXIPHENIDYLE
 3. GASTROESOPHAGEAL REFLUX:
METACLOPROPAMIDE, RANITIDINE.
 4. EXCESSIVE SALIVATION:
ATROPINE & BENZATROPINE for temporary relief.
 5. CONSTIPATION : Stool softeners and high fiber diet.
 ADHD : METHYLPHENIDATE.

21. SURGERY IN CP
 Ortho surgeon.
 Botulism toxin
 Posterior rhizotomy.
 Peacock technique in spastic case.
 Thalamotomy for Dyskinetic CP
 stem cell implantation giving promising results.
Patient can be fully rehabilitated.

22.  Parental counseling.
 Social awareness.
 Ultimate outcome
 Spastic Diplegia
 Hemiplegia
 Better prognosis
 Quadriplegic CP
 Choreoathetic CP

23. PREVENTION
 Good antenatal care.
 Fetal monitoring.
 Early C sections.
 Use of steroids to maturity of fetus.
 First 3 days after delivery:
INDOMETHACIN, ETHAMSYLATE, IM VITE.
CORTICOSTEROIDS :BETAMITHASONE.
 Neonatal Resuscitation.