Cerebral palsy results from damage to the developing brain, either before birth, during delivery, or in the first few years of life. It is the most common motor disability in childhood, affecting roughly 1 in 345 children in the United States. The vast majority of cases begin with something going wrong during pregnancy, though birth complications, premature delivery, infections, and even genetics all play a role.
Brain Damage Before Birth
Most cerebral palsy originates during pregnancy, when something disrupts normal brain development in the womb. The developing brain is especially vulnerable to two threats: reduced oxygen supply and infection. Both can damage the white matter that connects different brain regions, particularly the nerve pathways responsible for movement.
One of the most well-understood forms of this prenatal damage is called periventricular leukomalacia, a white matter injury most common in premature infants. When blood flow or oxygen to the brain drops, the result is a pattern of tissue death and inflammation in the white matter surrounding the brain’s fluid-filled chambers. This damages the nerve fibers that carry movement signals from the brain to the body, leading to the stiff, tight muscles characteristic of spastic cerebral palsy. Affected infants typically show signs like muscle stiffness, seizures, and developmental delays by six to nine months of age.
The placenta can also be a source of problems. When the placenta doesn’t function properly, the fetus may experience chronic oxygen deprivation. In some cases, blood clots or tissue fragments from a failing placenta travel into the fetal bloodstream and block vessels in the brain, causing a stroke before birth. Inflammation or infection in the placenta triggers a cascade of clotting and immune responses that can damage fragile blood vessels in the fetal brain. Cocaine use during pregnancy, for example, constricts the blood vessels supplying the uterus and can starve the fetus of oxygen.
Maternal Infections That Raise Risk
Certain infections during pregnancy can cross the placenta and damage the fetal brain directly, or trigger an inflammatory response that harms developing tissue. The CDC identifies several specific infections linked to cerebral palsy: chickenpox, rubella (German measles), and cytomegalovirus (CMV) among viruses, along with bacterial infections of the placenta, fetal membranes, or the mother’s pelvic region. These infections don’t always cause obvious illness in the mother, which is part of what makes them dangerous. The resulting inflammation can disrupt brain development even when the infection itself seems mild.
How Prematurity Multiplies the Risk
Premature birth is one of the strongest risk factors for cerebral palsy, and the earlier a baby is born, the greater the danger. A large meta-analysis broke this down by gestational age: babies born extremely early (before 28 weeks) face roughly 12 times the risk of cerebral palsy compared to full-term infants. Those born between 28 and 31 weeks have about 5.7 times the risk, and moderately preterm babies (32 to 36 weeks) still carry nearly double the risk.
The reason is straightforward. A premature baby’s brain is still in a critical stage of development. The white matter is especially fragile and poorly supplied with blood, making it highly susceptible to even brief drops in oxygen or blood pressure. The very systems meant to protect the brain from injury, like the ability to regulate blood flow, haven’t fully matured yet. This is why white matter injuries like periventricular leukomalacia are so closely tied to prematurity.
Birth Complications and Oxygen Deprivation
Birth asphyxia, where the baby’s brain is deprived of oxygen during labor and delivery, has long been considered a major cause of cerebral palsy. The actual picture is more complicated. Studies estimating the percentage of cerebral palsy cases caused by birth asphyxia range wildly, from less than 3% to over 50%, depending on how researchers define asphyxia and which cases they include. The wide range reflects genuine scientific uncertainty, but the takeaway is that difficult deliveries are only one piece of a larger puzzle. In many cases, the brain was already vulnerable before labor began due to prenatal factors like poor placental function or chronic oxygen deprivation.
That said, certain delivery emergencies clearly raise the risk. Prolonged labor, umbilical cord problems that cut off blood flow, placental abruption (where the placenta separates from the uterine wall), and severe drops in the baby’s blood pressure during birth can all cause the kind of acute brain injury that leads to cerebral palsy.
Genetic Factors
For years, cerebral palsy was thought of as purely an injury, something that happened to an otherwise healthy brain. Newer genetic research has changed that picture. Whole genome sequencing studies have found that genetic mutations account for a meaningful proportion of cerebral palsy cases. Researchers have identified at least 18 specific genes linked to cerebral palsy in multiple patients, many of which affect how brain cells develop, how nerve fibers form their protective coating, or how cells transport materials internally.
Some of these genetic factors work indirectly. Mutations in certain collagen genes, for instance, make blood vessels in the brain more fragile and prone to hemorrhagic stroke. Other genetic variations affect how the brain handles inflammation or recovers from oxygen deprivation, meaning a baby with certain gene variants might develop cerebral palsy from a level of stress that a genetically different baby would tolerate. Advanced paternal age has also been associated with increased risk, likely because older fathers pass on more spontaneous genetic mutations.
This doesn’t mean cerebral palsy is typically inherited in a simple pattern. Most of the identified mutations arise spontaneously rather than being passed down through families. But the genetic findings help explain why two babies can experience similar birth complications yet have very different outcomes.
Acquired Cerebral Palsy After Birth
A smaller number of cases develop after birth, when something damages a young child’s brain during the first few months or years of life. The NICHD lists several causes of acquired cerebral palsy:
- Infections like meningitis or encephalitis, which cause dangerous swelling and inflammation in the brain
- Stroke in infancy, caused by blood clotting disorders, abnormal blood vessels, congenital heart defects, or sickle cell disease
- Head trauma from car accidents, falls, or child abuse
Acquired cerebral palsy looks and functions the same as the congenital form. The brain damage is permanent, and the resulting movement difficulties are lifelong, though the specific pattern depends on which part of the brain was injured and how severely.
How Cerebral Palsy Is Recognized
Signs of cerebral palsy usually appear in the first few months of life, though many children aren’t formally diagnosed until age 2 or later. The earliest clues are developmental delays: a child who is slow to roll over, sit up, crawl, or walk. Before 6 months, a baby who can’t hold up their head when lifted from their back may be showing early signs. After 6 months, warning signs include difficulty rolling over, reaching with only one hand while keeping the other in a fist, or trouble bringing hands together. By 10 months, a child who crawls lopsidedly, scoots on their buttocks instead of crawling on all fours, or cannot stand even with support may need evaluation.
No single test confirms cerebral palsy. Doctors look at the full picture: the child’s movement patterns, muscle tone, reflexes, developmental history, and brain imaging results. The diagnosis is clinical, based on observing how the brain injury has affected the child’s ability to move and develop over time.