The major risk factors for cerebral palsy include premature birth, low birth weight, infections during pregnancy, oxygen deprivation around the time of delivery, and certain genetic mutations. About 1 in 345 children in the United States are identified with CP, and in most cases, the brain injury that causes it happens before or during birth rather than afterward.
CP results from abnormal brain development or damage to the developing brain, and rarely does a single factor act alone. Most cases involve a combination of risks that compound each other. Here’s what the evidence says about each one.
Premature Birth and Low Birth Weight
Prematurity is the single strongest risk factor for cerebral palsy. Babies born before 37 weeks have less time for their brains to develop in the protected environment of the womb, and the earlier a baby arrives, the higher the risk. The blood vessels supplying the brain in very premature infants are fragile and prone to bleeding, which can damage the surrounding tissue.
Low birth weight compounds this risk even among babies born at full term. A population-based study found that children classified as small for gestational age had 2.4 times the odds of developing CP compared to appropriately grown peers. Notably, the risk doesn’t suddenly spike at a clinical cutoff. It increases progressively as birth weight drops below the 50th percentile, meaning even moderately smaller babies carry some elevated risk.
Infections During Pregnancy
Certain maternal infections raise the likelihood of CP by triggering inflammation that can cross the placenta and affect the developing fetal brain. Urinary tract infections and other genital-urinary infections during pregnancy roughly double the risk, based on a large population cohort study. The timing matters: infections treated with antibiotics in the first trimester and genital-urinary infections in the third trimester showed the strongest associations.
The mechanism isn’t the infection itself reaching the baby’s brain in most cases. Instead, the mother’s inflammatory immune response releases signaling molecules that can interfere with normal brain development or damage vulnerable white matter tissue in the fetus.
Oxygen Deprivation Before or During Birth
Birth asphyxia, where the baby’s brain is temporarily deprived of adequate oxygen, has long been considered a primary cause of CP. The reality is more nuanced. Estimates of how many CP cases are actually caused by oxygen deprivation at birth range widely, from under 10% to over 30% depending on the study. Many cases previously blamed on difficult deliveries turn out to have had prenatal origins that were already in motion before labor started.
That said, oxygen deprivation remains a serious risk factor. Complications like umbilical cord problems, prolonged labor, or a sudden drop in the mother’s blood pressure can all reduce oxygen flow to the baby’s brain during critical minutes.
Placental Problems
The placenta is the baby’s lifeline for oxygen and nutrients, and when it malfunctions, the fetal brain is among the first organs affected. Chronic placental insufficiency, where the placenta gradually fails to deliver adequate blood flow, is linked to fetal growth restriction and carries an absolute CP risk exceeding 10% in extremely premature infants with growth abnormalities.
Placental dysfunction falls into two broad categories: vascular problems (reduced blood flow through the placental vessels) and inflammatory processes. Both can occur silently throughout pregnancy without obvious symptoms, which is one reason CP often has no single identifiable “moment” of injury.
Perinatal Stroke
A stroke in a newborn’s brain is one of the leading known causes of hemiplegic CP, the type that affects one side of the body. Perinatal strokes occur in roughly 1 in 3,000 live births and are often not detected at the time they happen. Many children appear healthy at birth and only show signs months later, when they begin favoring one hand or one side of the body during movement milestones.
These strokes can result from blood clots, abnormal blood vessel formation, or periods of reduced blood flow. Because symptoms may not appear until months after birth, perinatal stroke is likely underdiagnosed as a cause of CP.
Severe Newborn Jaundice
Most newborns develop mild jaundice, a yellowing of the skin caused by a buildup of bilirubin as the liver adjusts to life outside the womb. This is usually harmless. But when bilirubin levels climb extremely high and go untreated, the compound can cross into the brain and cause permanent damage, a condition called kernicterus.
A population-based study found that infants whose bilirubin levels rose significantly above the treatment threshold had 4.7 times the risk of CP compared to infants without elevated levels. The actual cases of CP consistent with kernicterus were rare and occurred only in infants who had at least two additional risk factors for brain toxicity, such as prematurity or enzyme deficiencies. In developed countries with routine newborn screening, this cause of CP has become uncommon but not eliminated.
Multiple Births and Assisted Reproduction
Twins, triplets, and other multiples face a higher CP risk primarily because multiple pregnancies are more likely to end in preterm delivery and low birth weight. Children conceived through assisted reproductive technology (ART) have about twice the overall rate of CP compared to naturally conceived children, at roughly 4 per 1,000 live births versus 2 per 1,000.
However, this elevated risk largely disappears when you compare like with like. Among single babies born at full term, the CP rate after ART was 1.52 per 1,000 versus 1.26 per 1,000 for natural conception, a difference that isn’t statistically meaningful. The real driver is that ART pregnancies are far more likely to produce multiples, and multiples are far more likely to arrive early. Preterm multiples conceived through ART had a CP rate of nearly 17 per 1,000.
Genetic Factors
For decades, CP was assumed to be almost entirely caused by environmental events like birth complications. Genomic research has shifted that picture. A study from the International Cerebral Palsy Genomics Consortium sequenced the genomes of 250 CP patients and their parents and found that roughly 14% of cases had identifiable genetic mutations playing a causal role.
About 12% of patients in the study carried mutations that arose randomly and were not inherited from either parent. Another 2% had mutations inherited from both parents, neither of whom had CP themselves. Two specific genes, FBXO31 and RHOB, were each individually sufficient to cause CP when mutated. When researchers introduced equivalent mutations into fruit flies, the insects developed movement difficulties resembling those seen in CP. Many of the implicated genes play roles in wiring brain circuits during early development, which helps explain why the resulting condition affects motor control so broadly.
The remaining 86% of cases in the study could involve environmental causes, subtler genetic variations that require larger studies to detect, or some interaction between the two.
Postnatal Causes in Infancy
A small percentage of CP cases originate after birth, typically within the first year or two of life. Brain infections like meningitis or encephalitis can cause the kind of damage that leads to CP. Traumatic head injuries from falls, car accidents, or physical abuse are another recognized cause. Bleeding within the brain, whether from injury or vascular abnormalities, can also destroy motor areas before they fully develop. These postnatal causes account for a minority of all CP cases, but they’re notable because some are preventable through injury prevention and prompt treatment of infant infections.