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.
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.
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
1.CONGENITAL CAUSES OF CEREBRAL PALSY
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
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
HAGBERGA - SWEEDISH
Half patients with spastic Diplegia had matrix hemorrhages
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 &
C. HYPOXIC ISCHEMIC DAMAGE-
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
INTERM INFANTS CAUSES OF HIE ARE MAINLY
b. Toxemia of pregnancy
c. Placental infarction
d. Intrauterine asphyxia
Results in cerebral Diplegia other spastic, dystonic,
D. Where a, b, c factors are not operative
RECENT STUDY OF COWAN & COLLEAGUES
MRI in neonatal encephalopathy excluding major
congenital malformations, chromosomal
80 % no established lesion or cerebral atrophy in
But in neonatal seizures 69% antenatal damage.
Clinical syndromes due to pathology: -
Matrix, hemorrhage, PVL, HIE, Kernicterus is Spastic
Hypoxic ischemic injury in term or preterm infants
take form of :
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.
MAJOR CONTROL & POSITVE DISORDERS
1. Spastic form
a. Spastic Quadriplegia
b. Spastic Diplegia
c. Spastic Hemiplegia.
2. Hypotonic form.
3. Ataxic form.
4. Dyskinetic form.
b. dystonic or both.
5. Mixed form
Spastic & choreoathetotic form
CLINICAL FEATURES & CLASSIFICATION
Mainly motor control disorders with accompanied symptoms.
2. Sensory visual hearing.
3. Communication defect.
4. Growth failure
6. Behavior & emotional problems.
a. attention deficit.
d. defective sexuality.
e. low self esteem.
H/O High risk infant.
H/O drug addiction in the mother.
MR or psychotic illness of mother.
see development mile stones:
Eyes, Ears, Musculoskeletal survey, Head
Observe early pointers to CP
Good antenatal care.
Early C sections.
Use of steroids to maturity of fetus.
First 3 days after delivery:
INDOMETHACIN, ETHAMSYLATE, IM VITE.