RISK FACTORS OF CEREBRAL PALSY

GENERAL
Gestational age < 32 weeks
Birth weight <2500 g
MATERNAL HISTORY
Mental retardation
Seizure disorder
Hyperthyroidism
Two or more prior fetal deaths
Sibling with motor deficits
DURING GESTATION
Twin gestation Chorionitis
Fetal growth retardation Increased urine protein excretion
Third-trimester bleeding Low placental weight
Premature placental separation
FETAL FACTORS
Abnormal fetal presentation
Fetal malformations
Fetal bradycardia
Neonatal seizures

ETIOLOGY
CP has multiple etiologies- many are still
unknown
Since CP is not a single entity, recurrence
risks depend on the underlying cause.
If there is a regression in skills, suspect a
degenerative disease.
ETIOLOGY
Most causes are prenatal- genetic,
congenital malformations, metabolic,
intrauterine infections, rather than perinatal
or postnatal- birth asphyxia, hemorrhage,
infarction, infections, trauma.


ETIOLOGY
Asphyxia
Asphyxia implies poor gas exchange, low Apgars and
neurologic depression during and soon after delivery.
Significant asphyxia is accompanied by acidosis.
Asphyxia is rarely the cause of CP in the term infant.
ETIOLOGY
Among the children with non quadriplegic
cerebral palsy, congenital disorders
appeared to account for about 1/3 of the
cases, and CNS infections accounted for 5%.



CP: ETIOLOGY
Brain injury can occur in the following periods:
a. Prenatal
b. Perinatal
c. Postnatal
PRENATAL PERIOD- wherein most causes of CP
occur.
TORCH infections
Intrauterine stroke
Genetic malformations
The most common currently understood causes
are related to brain injury occurring in children
born prematurely.


Very LBW infants increased risk of
periventricular hemorrhagic infarction
Periventricular hemorrhagic infarction
Hemorrhagic necrosis lateral to the external
angle of the lateral ventricle.
Of venous origin
Usually asymmetric
With healing Periventricular leukomalacia (
PVL) can develop.
Periventricular Leukomalacia
One of the strongest predictors of CP in the
premature neonate.
Almost always associated with a history of
prematurity.
PVL
Acute stage of periventricular
leukomalacia (PVL). Fluid-attenuated
inversion recovery (FLAIR) MRI shows
bilateral periventricular hyperintensity.
High signal on a T1-weighted image
obtained adjacent to the frontal horn
of the right lateral ventricle. This is
hemorrhagic periventricular
leukomalacia (PVL).
Extremely LBW infants:
Are also at increased risk
of CP.
Especially with a history of
resuscitation and
prolonged ventilation.
Protective factors: prenatal
care and steroids.

CP IN TERM INFANTS
Almost of children with CP were born term.
Cause of brain injury is often elusive.
Severe anoxic/ischemic brain injury:
Mechanical difficulties of the placenta
Umbilical cord
Actual delivery itself
Intrapartum asphyxia
Must be severe and prolonged to cause CP.
More global and more severe disability.

ETIOLOGY: POSTNATAL CEREBRAL INJURY AND
CP
Major causes:
CNS infections
Vascular causes
Head injury
Other Causes:
Anoxia
Ischemia
Inflammation

Primary unknown
Genetic hereditary
Metastatic
o 35% - lung
o 20% - breast
o 10% - kidney
o 5% - gastrointestinal tract
ETIOLOGY OF BRAIN
TUMOR
Often unknown
Under investigation:
o Genetic changes
o Heredity
o Errors in fetal development
o Ionizing radiation
o Electromagnetic fields (including cellular phones)
o Environmental hazards (including diet)
o Viruses
o Injury or immunosuppression
ETIOLOGY FOR
BRAIN TUMOR
PHYSICAL ASSESSMENT
General Appearance:
Patient was examining lying on bed febrile NIRD
EENT:
Pinkish Palpebral conjunctiva
(-) discharge
C/L: Equal chest expansion
Clear breath sounds
CVS: Adynamic pericardium
Regular rate and rhythm
Abdomen: flat, soft,
Extremeties: full pulses
CRT <2sec