Cerebral palsy (CP) results from damage to or abnormal development of the brain, typically before, during, or shortly after birth. About 1 in 345 children in the United States have CP, and while the causes vary widely, most cases trace back to something that went wrong during pregnancy rather than during delivery. In roughly 10% to 50% of cases, depending on the population studied, genetic factors play a significant role, and many cases still have no clearly identified cause.
Prenatal Brain Development Problems
The majority of cerebral palsy cases originate before a baby is born. During pregnancy, the fetal brain is extraordinarily sensitive to disruptions in blood flow, oxygen supply, and inflammation. When something interferes with normal brain development during those critical months, the resulting damage can affect the areas that control movement, posture, and coordination.
One key mechanism involves the placenta. The placenta is the baby’s lifeline for oxygen and nutrients, and when blood flow through it is impaired, the fetal brain can suffer. Reduced perfusion of the placenta from either the maternal or fetal side creates oxidative stress and oxygen deprivation. This can prime the developing brain for injury, so that even a relatively minor stress during labor could trigger damage that wouldn’t have occurred in a healthier pregnancy. Researchers describe this as an “acute upon chronic” pattern: a vulnerable brain, weakened by months of subtle stress, tips over into injury during or near delivery.
Fetal strokes are another prenatal cause. A blood clot, often originating from the placenta, can travel to the baby’s brain and block an artery. This cuts off blood supply to a specific region, killing brain tissue. The resulting damage can produce the one-sided weakness characteristic of hemiplegic CP.
Genetic Factors
For years, CP was viewed almost entirely as the result of environmental injuries to the brain. That picture has shifted dramatically. A large recent study found that about 24.5% of CP cases have an identifiable genetic basis, with researchers cataloging over 400 relevant genetic variants across 219 genes. Some of these genetic changes affect inflammation, blood clotting, or blood flow, which means they may not cause CP directly but instead make the developing brain more vulnerable to other insults.
Certain forms of CP show strong inheritance patterns. Ataxic CP (which primarily affects balance and coordination), symmetrical spastic CP, and CP accompanied by intellectual disability are the most likely to run in families. These forms are often inherited in an autosomal recessive pattern, meaning both parents carry one copy of the gene variant without being affected themselves. In one notable case, researchers identified a gene that only causes CP when inherited from the father, a rare pattern called genomic imprinting. That same gene’s activity can also be reduced by oxygen deprivation and low birth weight, illustrating how genetics and environment often overlap.
Infections During Pregnancy
Maternal infections are a well-established risk factor, though the danger isn’t always from the infection reaching the baby directly. When a pregnant person fights off an infection, the immune system releases inflammatory molecules called cytokines. These cytokines can cross into the fetal bloodstream and damage the developing brain’s white matter, the tissue that connects different brain regions and coordinates movement.
This inflammatory damage works through several pathways. Cytokines can disrupt fetal blood flow, cause tissue death in the brain’s white matter, and increase the permeability of the blood-brain barrier, allowing harmful substances to reach brain cells that are normally protected. The white matter is especially vulnerable in premature infants, which partly explains why preterm birth and infection together carry a compounded risk. Infections like cytomegalovirus (CMV), rubella, and toxoplasmosis are among the most concerning, but even common urinary tract infections or other bacterial infections during pregnancy can trigger enough inflammation to raise risk.
Premature Birth and Low Birth Weight
Being born too early is one of the strongest risk factors for CP. The earlier a baby arrives and the less they weigh, the higher the risk climbs. A Taiwanese population study quantified this starkly: compared to full-term infants, preterm babies weighing 1,000 to 1,499 grams (about 2.2 to 3.3 pounds) had 40 times the risk of developing CP. For the smallest preterm infants, those under 1,000 grams (roughly 2.2 pounds), the risk was nearly 63 times higher. In that smallest group, about 147 out of every 1,000 surviving babies developed CP.
The reason is straightforward: a premature brain is unfinished. The blood vessels supplying the brain are fragile and prone to bleeding. The white matter, still in active development, is highly susceptible to oxygen fluctuations and inflammation. Even with modern neonatal intensive care, very early and very small babies face substantial risks to their developing brains.
Oxygen Deprivation During Birth
Birth asphyxia, when a baby doesn’t get enough oxygen around the time of delivery, is probably the cause most people associate with CP. Its actual contribution is debated. Some studies estimate it accounts for fewer than 10% of cases, while others put the figure above 30%. The wide range reflects different definitions of asphyxia and different study populations.
Not every brief dip in oxygen during labor causes brain damage. The level of oxygen deprivation that leads to CP is severe. Clinical criteria for significant birth asphyxia include very low Apgar scores (the 0-to-10 rating of a newborn’s condition) persisting beyond five minutes, highly acidic blood from the umbilical cord, neurological symptoms like seizures or extreme floppiness, and signs that multiple organs have been affected. A baby who has a temporarily low heart rate during labor but recovers quickly is in a very different situation from one who experiences prolonged, severe oxygen deprivation.
It’s also worth noting that many babies diagnosed with birth asphyxia may have already been vulnerable before labor started due to placental problems, genetic factors, or chronic oxygen deficiency during pregnancy. What appears to be a birth injury sometimes reflects damage that was already underway.
Severe Jaundice in Newborns
Most newborns develop some degree of jaundice, a yellowish skin tint caused by the buildup of bilirubin as their liver adjusts to life outside the womb. This is usually harmless. But when bilirubin levels rise above 25 mg/dL and go untreated, the pigment can cross into the brain and damage the areas that control movement, a condition called kernicterus.
At bilirubin levels above 30 mg/dL, about one in seven infants will develop chronic kernicterus, which can cause a specific type of CP characterized by involuntary writhing movements. This is largely preventable. Phototherapy (treatment with special blue lights) is standard when bilirubin hits certain thresholds: 15 mg/dL or higher in babies 25 to 48 hours old, 18 mg/dL in babies 49 to 72 hours old, and 20 mg/dL in those older than 72 hours. In severe cases, a blood exchange transfusion is used. Kernicterus-related CP has become rare in countries with routine newborn screening, but it still occurs when jaundice is missed or undertreated.
Brain Injuries After Birth
A smaller but significant portion of CP cases develop after the newborn period, when an injury damages a previously healthy brain. This is called postneonatal or acquired CP, and it can result from events occurring anytime before age five. The three most common causes are traumatic brain injury, near-drowning, and meningitis (infection of the membranes surrounding the brain).
Meningitis caused by bacteria can trigger severe inflammation and swelling in the brain, destroying tissue in the motor areas. Near-drowning deprives the entire brain of oxygen, often damaging the regions most sensitive to oxygen loss, which include those controlling movement. Head injuries from falls, car accidents, or abuse can also cause the kind of localized or widespread brain damage that leads to CP. Because these causes are external and often preventable, car seat use, water safety, vaccination against bacterial meningitis, and safe sleep environments all play a role in reducing acquired CP.
Why Many Cases Have No Clear Cause
Despite advances in brain imaging and genetic testing, the cause of CP remains unknown in a large number of cases. This is partly because CP isn’t a single condition but a group of movement disorders with dozens of possible origins. In many children, the cause is likely a combination of factors: a genetic vulnerability that made the brain slightly more fragile, a subtle placental problem that reduced oxygen delivery by a small amount, and perhaps an inflammatory trigger that pushed the situation past a tipping point. No single factor was dramatic enough to be identified on its own, but together they were enough.
Diagnosis itself typically happens between 12 and 24 months of age in high-income countries, and as late as age five in places with fewer resources. Only about 21% of infants who will eventually be diagnosed receive that diagnosis by six months. This delay happens because many motor milestones, like sitting independently, aren’t expected until after six months, making it difficult to spot problems earlier. Earlier identification is an active area of focus, since beginning therapy sooner can improve outcomes even though the underlying brain injury itself doesn’t change.