Cerebral palsy

A non-progressive neurodevelopmental disorder affecting early motor development that characteristically impairs movement and posture.

Prevalence at approximately 2-3 per 1000 live births.

The incidence of cerebral palsy has not changed over the last 40 years despite widespread use of electronic fetal heart rate monitoring and higher Cesarean rate.

A congenital motor disability of cerebral origin.

Refers to a group of lifelong movement disorders.

While defind as a motor disorder it is often accompanied by intellectual deficits, epilepsy, and sensory disabilities.

Frequently accompanied by other neurodevelopmental disorders including: intellectual disability, epilepsy, and autism spectrum disorder.

The most common static encephalopathy.

Because of increased life expectancy individuals with cerebral palsy, the adult population with this disorder has been increasing associated with medical and social need.

Causes may be prenatal, perinatal, or postnatal.

The risk of cerebral palsy is lowest at 40 weeks, and highest risks are at 37 and 42 weeks later.

Gestational age at birth is associated with cerebral palsy, with prevalence among term infants about 1/40 the prevalence among extremely preterm survivors.

Increased CP risks among post-term births ( Blair E).

Risk is a U-shaped association with gestational age among infants reaching term.

It is possible that cerebral damage later noted to be cerebral palsy may disrupt time of delivery

It is a pervasive belief that birth asphyxia, secondary to adverse intrapartum events is the leading cause of cerebral palsy: large population-based studies show that birth asphyxia counts for less than 10% of cerebral palsy cases.
Increasing evidence suggests that a proportion of cerebral palsy cases may be secondary to rare genomic variants of large effect size, including copy number variants and single nucleotide variants,  as is the case of other neurodevelopmental disorders, such as intellectual disability, autism spectrum disorder, and epilepsy.
The rate of positive genomics findings ranges from 9 to 32%.

Causes include: perinatal strokes (13-37%), perinatal hypoxic-ischemic injury (6-28%), cerebral malformations (9-14%), cystic periventricular leukomalacia (5-10%), infections, chromosomal disorders and kernicterus.

Reported to be related to chorioamnionitis and fetal thrombotic vasculopathy.

Low Apgar scores, particularly, those recorded at age 5 minutes, greatly increase the risk for infants weighing greater than 2500 gm.

Patients have a lower weight and head circumference at birth, which suggest cerebral palsy influences differs from non-cerebral palsy infants even before birth.

Children with cerebral palsy 5 times as likely to have congenital malformations as children without CP.

93-95% of children with 5-minute Apgar score of 0 to 3 will not have CP therefore the vast majority of patients with CP do not have low Apgar scores.

Incidence increased in very low birth weight infants (20 per 1000 live births) compared to term infants (one per 1000 live births).

25-35% of children with cerebral palsy are born with a birth weight of <1500 gm.

Grade 3 to 4 intraventricular hemorrhage is a strong risk factor for later development of cerebral palsy.

Estimated 70-90% of cerebral palsy cases are due to prenatal factors and birth asphyxia a relatively minor role in about 10% of cases (Jacobsson B et al).

MRI abnormalities seen in 70-90% of cases.

Continuous electronic fetal monitoring to identify fetal asphyxia has not decreased the number of live births with cerebral palsy in the past three decades despite marked increase in surgical deliveries associated with such monitoring.

No cure presently exists.

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