Cerebral palsy (CP) develops when a baby’s brain is damaged or doesn’t develop normally during pregnancy, birth, or early childhood. In 85% to 90% of cases, the damage happens before or during birth. The remaining 10% to 15% of cases are acquired after birth, typically from an infection or injury in the first few years of life. Globally, CP affects roughly 1.6 out of every 1,000 live births.
Most Cases Begin Before Birth
The vast majority of cerebral palsy is congenital, meaning the brain damage occurs while the baby is still developing in the womb. This can happen in several ways. Sometimes the brain simply doesn’t form correctly during early pregnancy. Other times, an infection, a disruption in blood flow, or inflammation damages brain tissue that was developing normally.
One common form of prenatal brain injury involves the white matter near the brain’s fluid-filled chambers. When this tissue doesn’t get enough oxygen or blood, it softens and dies. White matter acts like the brain’s wiring system, carrying signals between different regions. When it’s damaged, the brain loses its ability to properly control muscles, which is the hallmark of CP.
Premature Birth and Low Birth Weight
Being born too early is one of the strongest risk factors. Babies born before 37 weeks of pregnancy have a higher chance of developing CP, and the risk climbs significantly for those born before 32 weeks. Premature babies are vulnerable because their brains are still in critical stages of development. The blood vessels supplying the brain are fragile at this stage and prone to bleeding or failing to deliver enough oxygen.
Low birth weight carries a similar risk. Babies weighing less than 5 pounds 8 ounces at birth face elevated odds, and those under 3 pounds 5 ounces face even greater risk. Prematurity and low birth weight often go hand in hand, but even full-term babies who are unusually small may be at increased risk.
Infections During Pregnancy
Certain infections in a pregnant person can cross the placenta and damage the developing baby’s brain. These infections trigger the release of inflammatory proteins that circulate through the baby’s blood and brain, causing injury even if the infection itself doesn’t directly reach the fetus.
The infections most closely linked to CP include cytomegalovirus (CMV), which is the most common congenital infection worldwide, as well as rubella (German measles), chickenpox, and toxoplasmosis. Bacterial infections of the placenta, fetal membranes, or the mother’s pelvic area also raise the risk. Timing matters: infections in the first trimester generally cause the most severe damage, because that’s when the brain’s foundational structures are forming.
CMV can cause growth restriction, hearing loss, and brain calcifications. Rubella can lead to heart defects, cataracts, and hearing loss alongside brain damage. Toxoplasmosis, often contracted from undercooked meat or cat litter, can cause calcifications inside the brain and eye damage. Any of these can result in the kind of motor-control problems that define cerebral palsy.
Oxygen Deprivation During Birth
Complications during labor and delivery can cut off the baby’s oxygen supply, damaging brain cells in a process sometimes called birth asphyxia. Placental detachment, uterine rupture, and umbilical cord problems are all potential triggers. When the brain is starved of oxygen and blood flow, cells begin to die within minutes.
The injury unfolds in two waves. The first wave happens immediately: without oxygen, brain cells can’t produce energy. Their internal machinery breaks down, they swell with fluid, and many die outright. A second wave of damage follows 6 to 48 hours later, driven by inflammation, toxic byproducts called free radicals, and a flood of stimulating brain chemicals that overexcite and kill additional neurons. This delayed second wave is why the full extent of brain injury from oxygen deprivation isn’t always apparent right away.
Jaundice and Newborn Complications
Jaundice, the yellowing of a newborn’s skin caused by a buildup of a waste product from broken-down red blood cells, is extremely common and usually harmless. But when severe jaundice goes untreated for too long, the waste product can cross into the brain and cause permanent damage, a condition called kernicterus. Kernicterus is a known cause of CP.
This is more likely when there’s a blood type mismatch between mother and baby, which causes the baby’s red blood cells to break down faster than normal. Routine newborn screening catches most cases of dangerous jaundice early, but kernicterus still occurs, particularly in settings with limited access to postnatal care.
Multiple Births and Fertility Treatments
Twins, triplets, and other multiples face a higher risk of CP than babies born from singleton pregnancies. Part of this comes down to the fact that multiples are more likely to be born premature and at lower birth weights. But the risk goes beyond prematurity alone. If one twin or triplet dies before or shortly after birth, the surviving baby’s risk of CP increases further, possibly due to changes in blood flow or inflammatory responses shared through the placenta.
Pregnancies conceived through assisted reproductive technology also carry a slightly higher chance of CP. This is partly because fertility treatments are more likely to result in multiple pregnancies, though some research suggests the risk is modestly elevated even in singleton pregnancies from these treatments.
Genetics Play a Larger Role Than Once Thought
For decades, CP was assumed to be entirely caused by environmental factors like oxygen deprivation or infection. That picture has shifted. Research published in Nature Genetics estimated that about 14% of all cerebral palsy cases may be linked to genetic factors, with roughly 12% traced to new mutations not inherited from either parent and another 2% linked to recessive gene variants. Many of these genes appear to control how brain circuits get wired during early development.
This doesn’t mean CP is a straightforward inherited condition in most families. The genetic mutations involved are often spontaneous, arising for the first time in the affected child. But it does mean that in a meaningful fraction of cases, the brain was vulnerable from the start because of its genetic blueprint, not solely because of an external event.
Acquired CP After Birth
The remaining 10% to 15% of cases develop after birth, usually within the first few years of life while the brain is still rapidly growing. Brain infections like meningitis and encephalitis can destroy tissue and leave lasting motor problems. Head injuries from falls, car accidents, or child abuse are another cause. Strokes in infants and toddlers, while rare, can also damage the motor areas of the brain and lead to CP.
Acquired CP is, in principle, more preventable than the congenital form. Car seats, vaccination against bacterial meningitis, and prevention of head trauma all reduce the risk. But once the brain damage has occurred, the resulting CP is permanent, just as it is with congenital cases.
How CP Is Detected
CP is not always obvious at birth. Many children are diagnosed between 12 and 24 months of age, when delays in motor milestones like sitting, crawling, or walking become apparent. However, earlier detection is now possible.
For infants younger than five months, a combination of a specialized movement assessment (which looks for specific spontaneous movement patterns called “fidgety movements”) and a brain MRI can predict CP with over 95% accuracy. For babies older than five months, a scored neurological exam combined with brain imaging predicts CP about 90% of the time. Earlier identification matters because it allows therapies to begin during the period when the infant brain is most adaptable, giving children the best chance of developing compensatory motor skills.
Why the Cause Often Stays Unknown
Even with modern imaging and genetic testing, doctors cannot pinpoint a specific cause in every case of CP. The brain can be injured in subtle ways during pregnancy that leave no obvious trail. A brief dip in blood flow, a mild infection that passed without symptoms, or a genetic variant that slightly disrupted brain wiring may all contribute without being easily detectable after the fact. Many cases likely result from a combination of factors rather than a single event. For families, this uncertainty can be frustrating, but it reflects the genuine complexity of how the brain develops over nine months of pregnancy and the first years of life.