Cerebral palsy is caused by abnormal brain development or damage to the developing brain, most often before or during birth. About 3 in every 1,000 children in the United States are identified with cerebral palsy, making it the most common motor disability in childhood. The damage typically affects areas of the brain that control movement, balance, and posture, and it can happen at several different stages: during pregnancy, during labor and delivery, or in the first few years of life.
What Happens in the Brain
The brain changes that lead to cerebral palsy fall into four main categories: damage to the brain’s white matter, a lack of oxygen reaching the brain, bleeding in the brain, and interrupted brain growth caused by gene changes. These aren’t different “versions” of cerebral palsy. They’re different types of injury that can all produce the movement and coordination problems associated with the condition.
The single most common form of brain damage behind cerebral palsy is periventricular white matter damage, which involves the death of white matter surrounding the fluid-filled ventricles deep inside the brain. White matter carries signals between brain regions, so when it’s destroyed, the brain loses its ability to properly relay movement commands to the body. This type of injury is especially likely in premature infants, whose brains are still forming the protective insulation around those white matter pathways.
Prenatal Causes: Before Birth
Most cerebral palsy originates during pregnancy, long before labor begins. The fetal brain is developing rapidly and is vulnerable to disruption from infections, reduced blood flow, or toxic exposures. Maternal infections such as cytomegalovirus (CMV), rubella, and toxoplasmosis can trigger inflammation that damages developing brain tissue. The infection doesn’t need to reach the fetus directly; the mother’s inflammatory immune response alone can be enough to interfere with fetal brain development.
Premature birth is one of the strongest risk factors. Children born before 37 weeks, and especially before 32 weeks, have a significantly higher chance of developing cerebral palsy. Their brains are at a stage where the white matter is particularly fragile and susceptible to injury from even minor changes in blood flow or oxygen levels. Low birth weight compounds the risk: babies weighing less than 5 pounds 8 ounces at birth face greater odds, and the risk climbs further for those under 3 pounds 5 ounces. Advances in neonatal intensive care mean more premature babies survive today than ever before, but survival sometimes comes alongside medical complications that raise cerebral palsy risk.
Birth Complications and Oxygen Deprivation
There’s a common assumption that cerebral palsy is usually caused by something going wrong during delivery, but the numbers tell a different story. Only about 14.5% of cerebral palsy cases are associated with oxygen deprivation during labor and delivery. That means the vast majority of cases originate either earlier in pregnancy or after birth.
That said, birth asphyxia remains a serious concern when it does occur. When a baby’s brain is deprived of oxygen during labor, the resulting injury is called hypoxic-ischemic encephalopathy (HIE). This affects roughly 2.5 out of every 1,000 live births in developed countries. Causes include umbilical cord problems, placental abruption (where the placenta separates from the uterine wall too early), prolonged or obstructed labor, and dangerously low maternal blood pressure. The severity of the brain damage depends on how long the oxygen deprivation lasts and how quickly it’s recognized and treated.
The Genetic Component
For decades, cerebral palsy was viewed purely as a result of physical injury to the brain. Genetics is now recognized as a meaningful contributor. Research published in Nature Genetics estimates that about 14% of cerebral palsy cases are linked to genetic factors, most involving mutations that affect how brain circuits become wired during early development.
About 12% of cases can be explained by de novo mutations, meaning genetic changes that appear spontaneously in the child rather than being inherited from either parent. Another 2% appear tied to recessive gene variants, where both parents unknowingly carry a weaker copy of a gene that, when doubled up, disrupts brain development. Several of the genes identified in this research control the construction of protein scaffolds that line neural circuits or guide how neurons extend and connect. In other words, these mutations don’t damage an already-formed brain. They cause it to wire up incorrectly in the first place.
This genetic connection is especially relevant for idiopathic cases, those with no identifiable injury or complication, which represent about 63% of cases studied. For many families who were told “we don’t know what caused it,” genetics may eventually provide an answer.
Causes After Birth
A small percentage of cerebral palsy cases are acquired after the newborn period, typically within the first two to three years of life while the brain is still developing rapidly. Brain infections like meningitis and encephalitis can destroy tissue and leave lasting motor damage. Severe head injuries from falls, car accidents, or child abuse are another cause. Strokes in young children, though rare, can also damage the motor areas of the brain and produce cerebral palsy.
Severe, untreated jaundice in newborns is another pathway. When bilirubin (a yellow pigment produced by the breakdown of red blood cells) builds to dangerously high levels, it can cross into the brain and cause a form of damage called kernicterus. This was once more common in cases of Rh incompatibility, where the mother’s immune system attacks the baby’s red blood cells. Routine screening and treatment have made this far less common, but it still occurs when jaundice goes unrecognized or untreated.
How Prevention Works
Because the causes are so varied, there’s no single way to prevent cerebral palsy. But several interventions have made a measurable difference. When preterm birth is anticipated before 32 weeks, administering magnesium sulfate to the mother reduces the risk of cerebral palsy in the baby by roughly 29%, according to pooled results from clinical trials reviewed by the American College of Obstetricians and Gynecologists. The treatment works by protecting the developing brain, though the exact mechanism isn’t fully understood.
Cooling therapy for newborns who experience oxygen deprivation during birth has also changed outcomes. When started within hours of birth, this treatment lowers the baby’s body temperature slightly to slow the cascade of brain damage that follows oxygen loss. Vaccinations against rubella, improved prenatal care to detect and manage infections, Rh screening during pregnancy, and newborn jaundice monitoring all target specific causes on the list. None of these eliminates cerebral palsy entirely, but together they’ve reduced the rate of preventable cases.
Why Many Cases Have No Clear Cause
Despite everything known about risk factors and mechanisms, a large portion of cerebral palsy cases still have no single identifiable cause. The majority of cases in research studies are classified as idiopathic. This doesn’t mean nothing happened. It usually means the cause was some combination of subtle genetic vulnerability, minor prenatal events, or disruptions too small to detect on imaging but significant enough to alter how the brain developed. As genetic testing becomes more sophisticated, that “unknown” category is expected to shrink, giving more families a clearer picture of what happened and why.