The vast majority of cerebral palsy cases, between 85% and 90%, originate before or during birth rather than afterward. During pregnancy, the developing brain is vulnerable to a surprisingly wide range of disruptions: infections, reduced blood flow through the placenta, strokes, genetic mutations, and inflammatory responses that damage neurons before a baby takes their first breath. Understanding these causes can feel overwhelming, but they fall into a handful of distinct categories.
Placental Problems and Oxygen Deprivation
The placenta is the fetus’s lifeline for oxygen and nutrients, and when it fails to deliver enough of either, the developing brain pays the price. Placental insufficiency is the leading cause of fetal growth restriction, creating a state of chronic low oxygen that forces the fetus to redirect blood flow toward the brain and away from other organs. This compensatory response, called “brain sparing,” sounds protective but doesn’t fully work. Even with brain sparing, affected infants show delayed development of the brain’s insulating white matter and measurable changes in brain organization that persist into childhood.
Placental abruption, where the placenta partially or fully separates from the uterine wall, cuts off blood flow more abruptly and can cause both stroke and widespread oxygen deprivation. The white matter surrounding the brain’s fluid-filled chambers is especially vulnerable. In animal studies of fetal growth restriction, researchers have documented up to a 20% reduction in the protective coating around nerve fibers in parts of the brain, along with inflammation and direct damage to nerve cell extensions. These injuries to white matter are the same type of damage seen in many children later diagnosed with cerebral palsy.
Maternal Infections That Reach the Fetal Brain
Certain infections during pregnancy can cross the placenta and directly attack fetal brain tissue. The group of pathogens most strongly linked to brain damage is known as TORCH: toxoplasmosis, rubella, cytomegalovirus (CMV), herpes simplex, and others. These pathogens are drawn to the fetal brain because of the intense metabolic activity of developing nerve and support cells, and they can cause lasting damage even in babies who appear healthy at birth.
CMV is one of the most common culprits. The virus replicates in the tissue lining the brain’s fluid-filled spaces and in the region where new neurons are generated. It also targets the cells lining blood vessels, which can trigger small blood clots and inflammation in the vessel walls. This leads to tiny areas of dead tissue (calcifications), cysts near the brain’s ventricles, and sometimes bleeding within the brain itself. The timing of infection matters enormously: an early pregnancy infection disrupts the production of new neurons entirely, while a later infection allows normal neuron numbers but impairs how those neurons organize and connect.
Toxoplasmosis, caused by a parasite commonly found in undercooked meat and cat feces, produces a different pattern of damage. It tends to block the narrow passage that drains fluid from the brain, leading to a dangerous buildup of pressure (hydrocephalus). It also causes widespread calcifications in deep brain structures like the basal ganglia and thalamus, areas critical for movement control.
Inflammation Without Direct Infection
A maternal infection doesn’t have to reach the fetal brain directly to cause harm. When a pregnant person fights off an infection anywhere in the body, the immune system releases signaling molecules called cytokines. These molecules are essential for fighting illness, but they also cross the placenta and trigger inflammation in fetal brain tissue. Chorioamnionitis, an infection of the membranes surrounding the fetus, is a well-documented example. Even when the mother shows no symptoms, the resulting inflammation has been linked to both fetal stroke and white matter injury.
This inflammatory pathway helps explain why conditions seemingly unrelated to the brain, like a urinary tract infection or a dental abscess during pregnancy, have been associated with increased cerebral palsy risk in large population studies. The damage comes not from the pathogen itself but from the body’s immune response spilling over to the developing fetal nervous system.
Fetal Stroke
Strokes can happen before birth, cutting off blood supply to parts of the developing brain and causing the same type of tissue death seen in adult strokes. Several pregnancy-specific factors raise the risk. Pregnancy itself is a naturally pro-clotting state: levels of multiple clotting factors rise significantly while the body’s ability to dissolve clots decreases. This protects against hemorrhage during delivery but also makes abnormal clots more likely.
Preeclampsia reduces blood flow through the placenta and can send clot fragments or reduce overall blood supply to the fetal brain. Gestational diabetes and pregnancy-induced hypertension carry similar risks. On the fetal side, inherited clotting disorders play a role. Elevated levels of a blood protein called lipoprotein(a) are considered the most important clotting risk factor in newborns. Genetic variants affecting clotting proteins like Factor V Leiden and prothrombin also increase risk. Babies born with congenital heart defects face additional stroke risk from abnormal blood flow patterns that can send clots to the brain.
Cocaine use during pregnancy deserves specific mention because it causes blood vessel constriction and spasm, directly increasing the chance of fetal stroke.
Genetic Causes
For years, cerebral palsy was assumed to result almost entirely from oxygen deprivation or injury. More recent genetic research has changed that picture substantially. Studies using advanced gene sequencing have identified at least 18 genes and 5 chromosomal regions with strong evidence for causing cerebral palsy directly, independent of any birth injury.
Different genetic mutations tend to produce different movement patterns. Mutations in genes involved in nerve cell structure and signaling are linked to spastic cerebral palsy, the most common type, where muscles are stiff and tight. Mutations affecting the basal ganglia, a brain region that helps coordinate smooth movement, are found in children with the involuntary writhing movements of choreoathetoid cerebral palsy. Mutations in genes controlling calcium channels and neurotransmitter release have been identified in children with the balance and coordination problems of ataxic cerebral palsy.
These findings mean that some cases previously attributed to birth complications may actually have had a genetic origin. This doesn’t change the child’s experience or treatment, but it can matter for family planning and for understanding why cerebral palsy sometimes occurs in pregnancies with no obvious complications.
Rh Incompatibility and Severe Jaundice
When a mother’s blood type is Rh-negative and the baby’s is Rh-positive, the mother’s immune system can attack the baby’s red blood cells. This produces a flood of bilirubin, a yellow waste product from broken-down blood cells. In high concentrations, bilirubin is fat-soluble and crosses into the brain, where it has a particular affinity for the globus pallidus, hippocampus, and subthalamic nucleus, all structures involved in movement and memory.
Once inside brain cells, bilirubin damages the energy-producing structures (mitochondria), disrupts normal cell function, and triggers cell death. It also interferes with the growth of nerve cell connections. If untreated, this condition, called kernicterus, progresses over several years into choreoathetoid cerebral palsy, characterized by involuntary, twisting movements. Routine Rh screening and preventive treatment during pregnancy have made this cause far less common, but it still occurs when prenatal care is delayed or unavailable.
Twin and Multiple Pregnancies
Carrying more than one baby significantly increases cerebral palsy risk. Multiples have a cerebral palsy rate of about 7 per 1,000 live births compared to 1.6 per 1,000 for singletons, a roughly fourfold increase in risk. The reasons are layered: multiples are far more likely to be born prematurely, to experience growth restriction from shared placental resources, and to face complications like twin-to-twin transfusion syndrome, where blood flow between twins sharing a placenta becomes unbalanced. If one twin dies in the womb, the surviving twin faces an especially high risk of brain injury from sudden changes in blood pressure and blood flow.
Maternal Health Conditions
Certain chronic conditions in the pregnant person are associated with higher cerebral palsy risk in their child. Thyroid disorders identified during pregnancy have been linked to a threefold increased risk of unilateral spastic cerebral palsy, the type affecting one side of the body. Preeclampsia and gestational diabetes contribute to cerebral palsy risk primarily through their effects on placental function and fetal blood flow, as described above.
Protective Measures During Pregnancy
For pregnancies at risk of very early preterm delivery, one intervention has strong evidence for reducing cerebral palsy risk. Magnesium sulfate, given intravenously to the mother before delivery at less than 32 weeks of gestation, reduces the child’s risk of cerebral palsy by about 32%. International guidelines recommend starting it when preterm birth is expected within 24 hours, ideally at least 4 hours before delivery, though shorter windows still offer some benefit. The treatment is recommended regardless of the reason for preterm birth or the number of babies being carried. On average, treating 41 women prevents one case of cerebral palsy or death, making it one of the most effective neuroprotective strategies available in obstetrics.
Beyond magnesium sulfate, standard prenatal care addresses many of the causes outlined above: Rh screening prevents most cases of severe jaundice-related brain injury, infection screening and treatment reduce inflammatory exposure, and monitoring for preeclampsia and growth restriction allows timely delivery before prolonged oxygen deprivation causes irreversible damage.