CAUSES :
. 70% of the time, neither causes nor risk factors can be identified
. In utero bacterial infections (chorioamnionitis), viral infections (e.g. rubella),CNS, malformations, chromosomal abnormalities, coagulation disorders, kernicterus, CNS trauma and intraventricular hemorrhage
. While most cases are due to prenatal events and prematurity, 10% or less of cases are due to intrapartum events. Such cases are almost always of spastic quadriplegic type or dyskinetic type and are associated with
evidence of severe metabolic acidosis at birth (pH . 7.00) and early onset neonatal encephalopathy at birth. Criteria which individually are nonspecific but which
together suggest intrapartum cause include a sentinelhypoxic event immediately before or during labor (e.g. cord prolapse, abruption or uterine rupture); sudden, rapid and sustained deterioration of the fetal heart rate pattern which was previously normal; Apgar scores
of . 6 for greater than fi ve minutes; early evidence of multisystem involvement and early imaging showing acute cerebral abnormality.
--------------------------------------------------------------------------
DIFFERENTIAL DIAGNOSIS :
Cerebral palsy is a descriptive term based on clinical observation. Chromosomal and metabolic abnormalities must be excluded. Early diagnosis made at 12 months of life may be wrong more than half the time. Evidence
of disease progression excludes cerebral palsy. Early warning signs include delay in motor milestones, toe walking, persistent fisting, seizures, irritability, poor suck, established handedness before 2 years of age, and abnormal limb posture.
• Laboratory data is not required to make the diagnosis.
• Other tests may help exclude Tay-Sachs metachromatic leukodystrophy, mucopolysaccharidosis
SPECIAL TESTS :
• Urine amino acid screening
• High resolution karyotype
DIAGNOSTIC PROCEDURES :
• History and careful physical exam
• Pedigree
• EEG, MRI, CT