Cerebral palsy (CP) results from damage to the developing brain, most often before or during birth. About 1 in 345 children in the United States are affected. Despite a common assumption that something goes wrong during delivery, the brain injury behind CP usually begins well before labor starts, and only about 14.5% of cases in normal-weight infants are linked to oxygen deprivation during birth.
What Happens in the Brain
CP is not a single event but the outcome of injury to parts of the brain that control movement. The damage typically targets the white matter near the fluid-filled ventricles deep in the brain. This area is especially vulnerable because it sits in a “watershed zone” between two arterial blood supplies. When blood flow drops, this region is the first to suffer.
The cells most at risk are oligodendrocytes, the support cells responsible for wrapping nerve fibers in a protective coating called myelin. Without that coating, the long nerve pathways that carry movement signals from the brain to the muscles cannot develop or function properly. The motor pathways that control the arms and legs run directly through this periventricular region, which is why movement is the hallmark symptom of CP.
Two specific injuries account for most cases in premature infants. Periventricular leukomalacia (PVL) is underdeveloped or damaged white matter in this area, and it is the leading cause of CP in preterm babies. Intraventricular hemorrhage (IVH) is bleeding from fragile developing blood vessels in the brain, which can itself trigger PVL or cut off blood flow to other regions.
Premature Birth Is the Strongest Risk Factor
The earlier a baby is born, the higher the risk. Compared to babies born at 39 to 40 weeks, those born at 22 to 24 weeks are roughly 47 times more likely to develop CP. The risk drops steadily with each additional week of pregnancy but remains elevated even for late preterm births: babies born at 35 to 36 weeks still face about twice the risk, and those born at 37 to 38 weeks carry a 30% higher risk than full-term infants.
For the earliest preterm babies, neonatal complications explain the vast majority of that elevated risk. At 24 weeks, about 92% of the increased CP risk is accounted for by complications like bleeding in the brain, infections, and breathing problems. By 32 weeks that proportion drops to about 46%, and by 36 weeks it falls to around 16%, meaning other factors play a larger role as gestational age increases.
Prenatal Causes: Infection, Blood Flow, and Inflammation
Infections during pregnancy are one of the most important prenatal pathways to CP. Viruses like cytomegalovirus (CMV), rubella, and chickenpox, along with bacterial infections of the placenta, fetal membranes, or the mother’s pelvis, can trigger a flood of inflammatory proteins called cytokines. These cytokines are directly toxic to the immature oligodendrocytes that build myelin. The result is white matter that never develops properly, even if the baby is born at full term.
Anything that reduces blood flow to the fetal brain can also cause damage. Placental problems, blood clots, and conditions that lower the mother’s blood pressure or oxygen levels may all contribute. Because the developing brain already operates with relatively low blood flow, even a modest drop can be enough to injure vulnerable tissue.
Birth Complications and Oxygen Deprivation
Oxygen deprivation during labor and delivery gets the most public attention, but it accounts for a relatively small share of CP cases. Research on normal-birth-weight infants found that only about 14.5% of spastic CP cases were associated with oxygen loss during birth. In many of those cases, prenatal factors had already made the brain more vulnerable before labor began.
That said, severe oxygen deprivation during delivery is one of the more preventable causes. Complications like a prolapsed umbilical cord, placental abruption (when the placenta separates from the uterine wall too early), or prolonged difficult labor can starve the brain of oxygen long enough to cause lasting injury. When this happens, the damage tends to affect deeper brain structures involved in coordinating movement.
Severe Jaundice After Birth
Newborn jaundice is common and usually harmless, but when bilirubin (the yellow pigment the body produces as it breaks down red blood cells) climbs to extreme levels and goes untreated, it becomes toxic to the brain. This condition, called kernicterus, can cause a specific form of CP along with hearing loss and vision problems. Healthy full-term newborns older than 72 hours typically have bilirubin levels below 17 mg/dL; cases of kernicterus have involved levels exceeding 35 mg/dL on average. Kernicterus is almost entirely preventable with routine bilirubin screening and phototherapy.
Acquired CP in Infancy and Early Childhood
A small number of children develop CP after the newborn period, typically from brain damage that occurs in the first few months or years of life. This is called acquired cerebral palsy, defined as beginning more than 28 days after birth. Causes include:
- Infections like meningitis or encephalitis that inflame the brain or its surrounding membranes
- Stroke or blood flow problems from clotting disorders, abnormal blood vessels, congenital heart defects, or sickle cell disease
- Head injuries from car accidents, falls, or child abuse
The Role of Genetics
CP has traditionally been viewed as the result of environmental brain injury, but genetic factors play a larger role than previously thought. Researchers have identified at least 55 genes linked to CP, with mutations found in individual genes, larger chromosomal deletions, and mitochondrial DNA. The most frequently implicated genes are associated with conditions like hypomyelinating leukodystrophies (diseases where myelin fails to form properly), metabolic disorders, hereditary spastic paraplegias, blood clotting disorders, and problems with neurotransmitter production.
A genetic contribution does not mean CP is typically inherited in a straightforward way. In most cases, these mutations arise spontaneously rather than being passed down from parents. But their discovery helps explain why some children develop CP without any obvious pregnancy or birth complication. Certain clinical features, such as CP with intellectual disability, epilepsy, or brain imaging that looks normal, may point toward a genetic cause worth investigating.
How CP Is Identified
CP is generally diagnosed during the first or second year of life. Children with mild symptoms may not receive a confirmed diagnosis until they are a few years older. The American Academy of Pediatrics recommends developmental screening at 9 months (when many movement issues become visible), 18 months (when mild delays are easier to spot), and 24 or 30 months (when most movement delays can be detected).
Parents often notice the earliest signs themselves: a baby who favors one side of the body, seems unusually stiff or floppy, or misses milestones like sitting, crawling, or walking. Brain imaging, typically an MRI, can reveal the white matter injury or structural differences that confirm the diagnosis and help clarify the underlying cause.