Cerebral palsy is caused by abnormal brain development or damage to the developing brain, either before, during, or shortly after birth. No single event is responsible in most cases. Instead, a combination of risk factors typically contributes, and in many children, the exact cause is never pinpointed with certainty. The overall incidence has been declining, dropping roughly 50% between 2006 and 2024, likely due to improvements in prenatal care and neonatal medicine.
Premature Birth Is the Strongest Risk Factor
Being born too early is the single biggest predictor of cerebral palsy. The earlier a baby arrives, the higher the risk, because the brain is still forming critical structures, particularly the white matter that coordinates movement. A large population-based study in Taiwan quantified this sharply: among babies born at term, cerebral palsy occurred in about 2.5 per 1,000 survivors. For preterm babies with low birth weight, that rate jumped to nearly 28 per 1,000. For the smallest preterm babies (under about 2.2 pounds), it reached 147 per 1,000, a risk roughly 60 times higher than full-term infants.
The vulnerability comes down to timing. The white matter surrounding the brain’s fluid-filled ventricles is especially fragile in premature infants. Injury to this tissue, called periventricular white matter injury, is the most common form of brain damage in preterm babies and the leading cause of cerebral palsy in this group. Even brief disruptions in blood flow or oxygen delivery can damage cells that are still migrating to their final positions in the brain.
What Happens Before Birth
Most cerebral palsy originates during pregnancy, not during delivery. The developing brain can be disrupted by problems with blood flow through the placenta, infections, or genetic factors that alter how brain cells grow and connect.
When the placenta doesn’t deliver enough blood, the fetus doesn’t get adequate oxygen and nutrients. This is common in pregnancies complicated by high blood pressure or other conditions that restrict placental blood flow. Babies affected by this kind of growth restriction show measurable differences in brain structure: reduced gray matter volume, fewer brain cells overall, and altered blood flow patterns in the brain. In some cases, a fetal stroke, a blood clot or bleed in the brain before birth, can destroy tissue and leave permanent damage.
Infections during pregnancy are another major contributor. When a pregnant person develops an infection, the immune response sends inflammatory signals across the placenta to the fetus. These signals can directly injure developing brain cells, disrupt the growth of the insulating coating around nerve fibers, and trigger a cascade of toxic byproducts. This process doesn’t require the infection itself to reach the baby. The mother’s inflammatory response alone can cause harm. Infections linked to this risk include common ones like urinary tract infections and respiratory infections, as well as more specific pathogens like cytomegalovirus, syphilis, rubella, herpes simplex, and Zika virus. Inflammation of the placental membranes, a condition called chorioamnionitis, is a particularly well-documented pathway to fetal brain injury.
Genetics Play a Larger Role Than Previously Thought
For decades, cerebral palsy was assumed to be almost entirely caused by physical injury to the brain. Research over the past ten years has challenged that assumption. Genetic testing has revealed that a meaningful percentage of children with cerebral palsy carry spontaneous gene mutations, ones that weren’t inherited from either parent but arose randomly during development.
In one study of children with cerebral palsy affecting one side of the body, about 7% had newly occurring genetic changes or sex chromosome abnormalities. These mutations affected genes involved in building brain structure, forming connections between nerve cells, and producing key proteins for brain development. Another 19% carried rare inherited genetic variations linked to known neurological conditions. The CDC notes that cerebral palsy with a genetic basis is not preventable, which underscores why identifying these cases matters for families seeking answers.
Oxygen Deprivation During Birth
Oxygen deprivation around the time of delivery is probably the most widely known cause of cerebral palsy, but it accounts for a smaller share of cases than most people assume. When it does occur, the pattern is distinctive. A prolonged drop in oxygen and blood flow damages specific brain regions, and MRI scans later show a characteristic injury pattern.
One study published in Neurology found that among term-born children who developed cerebral palsy and had MRI findings consistent with oxygen deprivation during birth, about 82% had shown clear signs of distress as newborns. But roughly one in six did not, meaning some babies sustained this type of injury without obvious symptoms at birth. This is significant because it suggests that oxygen-related brain damage can sometimes go unrecognized in the immediate newborn period.
Severe Jaundice and Newborn Brain Damage
Newborn jaundice is extremely common and usually harmless. But when bilirubin, the yellow pigment that causes jaundice, rises to very high levels and goes untreated, it can cross into the brain and cause permanent damage. This condition is called kernicterus, and it can lead to a specific type of cerebral palsy that primarily affects movement coordination.
The actual risk is very low. A population-based study found that kernicterus-related cerebral palsy occurred in only about 0.57 per 100,000 births. Critically, every affected infant had bilirubin levels far above the threshold for treatment and at least two additional risk factors for brain toxicity, such as prematurity, a genetic enzyme deficiency, or oxygen deprivation. Among babies with mildly elevated bilirubin, the excess risk of cerebral palsy was minimal. Routine newborn screening for jaundice has made this cause increasingly rare in countries with good neonatal care.
Brain Injuries After Birth
A small percentage of cerebral palsy cases develop after a baby is born healthy. The most common postnatal causes are infections that reach the brain, particularly meningitis and encephalitis during the first months of life. These infections cause swelling and inflammation that can destroy brain tissue responsible for movement control.
Head injuries from accidents, near-drowning events, and child abuse (particularly shaken baby syndrome) can also cause the kind of brain damage that leads to cerebral palsy. These postnatal causes are distinct because the brain was developing normally before the injury occurred, and the damage tends to be more localized than prenatal causes.
Multiple Births Carry Extra Risk
Twins, triplets, and other multiples face a higher risk of cerebral palsy than singletons. Several factors overlap to explain this. Multiple pregnancies are far more likely to end in premature delivery, and as noted above, prematurity is the strongest individual risk factor. Multiples also tend to have lower birth weights even when carried closer to term. In twin pregnancies specifically, the death of one twin in utero can trigger inflammatory and circulatory changes that injure the surviving twin’s brain.
Why Many Cases Have No Clear Cause
Despite advances in imaging and genetic testing, many families never receive a definitive explanation for their child’s cerebral palsy. This is because the condition often results from a combination of factors rather than a single event. A baby might carry a genetic vulnerability that makes their brain slightly more susceptible to injury, then experience mild oxygen stress during delivery that a more resilient brain would have tolerated. Neither factor alone would have caused cerebral palsy, but together they cross a threshold.
The declining incidence of cerebral palsy, from about 4.3 per 1,000 live births in 2005 to 2.5 per 1,000 in 2020, suggests that better prenatal monitoring, improved management of premature infants, and advances like cooling therapy for newborns with oxygen deprivation are making a difference. But the condition has not been eliminated, in part because some of its causes, particularly genetic ones, are not yet preventable.