Cerebral palsy (CP) develops when something damages or disrupts the developing brain, either before birth, during delivery, or in the first years of life. About 85% to 90% of cases are congenital, meaning the brain injury happens before or during birth. The remaining 10% to 15% are acquired after birth. In the United States, roughly 1 in 345 children are identified with CP.
Brain Damage Before Birth
The most common window for the brain injury behind CP is during pregnancy, when the fetal brain is rapidly forming and highly vulnerable. Several things can go wrong during this period.
Infections in the mother are a well-established risk. Viruses like chickenpox, rubella (German measles), and cytomegalovirus (CMV) can cross the placenta and damage developing brain tissue. Bacterial infections of the placenta, fetal membranes, or the mother’s pelvic area also raise the risk. These infections trigger inflammation that can interfere with normal brain development or directly injure brain cells.
Problems with the placenta play a significant role as well. When the placenta separates from the uterine wall too early (placental abruption), it cuts off the baby’s blood and oxygen supply. Research on pregnancies complicated by placental abruption found that 100% of the babies who developed CP had severely acidic cord blood at delivery, a sign of prolonged oxygen deprivation. Smoking during pregnancy, alcohol consumption, high blood pressure, and having had multiple prior deliveries all increase the risk of abruption leading to CP.
Certain maternal health conditions also matter. Thyroid disorders identified during pregnancy are linked to roughly a threefold increase in the risk of one specific type of CP (unilateral spastic CP, which affects one side of the body). The connection likely involves changes in blood clotting that can cause small strokes or bleeding events in the fetal brain.
What Happens During Oxygen Deprivation
When a baby’s brain loses its oxygen supply, the damage unfolds in two waves. The first wave happens immediately: without oxygen and glucose, brain cells can’t produce enough energy to maintain their basic functions. The pumps that keep cells stable fail, and toxic levels of calcium flood into neurons. This triggers swelling and begins killing brain tissue.
A second wave of damage follows 6 to 48 hours later, driven by inflammation and a continued cascade of cell death. The areas most affected include regions that control movement, coordination, and muscle tone, which is why CP primarily shows up as a movement disorder. The specific pattern of brain injury determines which type of CP a child develops and which parts of the body are affected.
Premature Birth Is the Strongest Risk Factor
Babies born early face dramatically higher odds of CP. The brain of a premature infant is especially fragile, with blood vessels and white matter that are vulnerable to bleeding and oxygen fluctuations. Among babies born before 27 weeks of gestation, nearly 1 in 5 (18.8%) are later diagnosed with CP. That rate is striking compared to the general population, where CP occurs in roughly 3 out of every 1,000 births.
Birth weight tells a similar story. CP is 70 times more common in infants weighing less than 3.3 pounds at birth. Concerningly, a large study tracking extremely preterm infants from 2008 through 2019 found that the odds of CP in this group increased by an average of 11% per year over that period, likely because more extremely premature babies are now surviving but remain at high risk for brain injury.
Complications During Labor and Delivery
A difficult delivery can deprive the baby’s brain of blood flow and oxygen at a critical moment. Prolonged labor, umbilical cord problems (such as the cord wrapping around the neck or becoming compressed), and emergency situations like uterine rupture can all interrupt oxygen delivery. When the interruption is severe enough, it causes what doctors call hypoxic-ischemic encephalopathy, the formal term for brain injury from oxygen deprivation around the time of birth.
Not every complicated delivery leads to CP. The brain can tolerate brief interruptions in oxygen. It’s sustained deprivation, lasting long enough to trigger the two-phase injury process described above, that causes permanent damage. Cooling therapy, where a newborn’s body temperature is lowered shortly after birth, is now a standard treatment to slow the second wave of brain injury and reduce the extent of damage.
Brain Injuries After Birth
The 10% to 15% of CP cases classified as acquired happen when something damages a young child’s brain after birth, typically in the first few years of life. The most common causes include:
- Infections: Meningitis and encephalitis (infections of the brain or its surrounding membranes) can cause widespread brain damage in infants and toddlers.
- Head trauma: Serious injuries from falls, car accidents, or abusive head trauma (shaken baby syndrome) can damage the motor areas of the brain.
- Stroke: Blood clots or bleeding in the brain can occur even in very young children, destroying tissue in areas that control movement.
- Severe jaundice: When newborn jaundice goes untreated, bilirubin (the yellow pigment that causes the skin discoloration) can build up to toxic levels and penetrate the brain, permanently damaging regions involved in movement and coordination.
The Role of Genetics
CP has traditionally been viewed as something caused entirely by environmental events like oxygen deprivation or infection. But genetic research is changing that picture. Studies using whole-genome sequencing have identified specific gene mutations in a meaningful proportion of children with CP, particularly in cases where no clear environmental cause was found.
Some of these genes directly disrupt early brain development, causing structural problems that lead to CP symptoms. Others work more indirectly: they make a baby’s brain more vulnerable to the kinds of environmental insults that cause CP. For example, mutations in the COL4A1 and COL4A2 genes increase susceptibility to bleeding in the brain, while a chromosomal deletion called 1p36 deletion syndrome can cause low muscle tone before birth, leading to delivery complications and oxygen deprivation.
Researchers have now identified more than 20 genes and chromosomal regions with strong evidence of contributing to CP. Most of these are linked to the spastic type, which is the most common form. Genetics doesn’t explain the majority of CP cases, but it’s an increasingly recognized piece of the puzzle, especially for families where no obvious birth injury or infection occurred.
Why the Cause Often Isn’t a Single Event
For many children with CP, there isn’t one clean explanation. A baby might carry a genetic vulnerability that makes their brain slightly more fragile, then be born a few weeks early, then experience a brief period of oxygen deprivation during delivery. None of those factors alone would necessarily cause CP, but together they cross a threshold. This is why identifying the exact cause of a child’s CP can be difficult, and why many families never receive a single definitive answer. The brain injury that causes CP is often the result of multiple risk factors converging during a period when the developing brain is at its most vulnerable.