Most cases of cerebral palsy originate before birth, when something disrupts normal brain development in the womb. The causes range from infections and oxygen deprivation to genetic mutations and inflammatory responses, often overlapping in ways that make pinpointing a single trigger difficult. Understanding these prenatal causes can help clarify what happens during fetal brain development and why certain pregnancies carry higher risk.
Oxygen Deprivation From Placental Problems
The placenta is the fetus’s lifeline for oxygen and nutrients. When it doesn’t function properly, a condition called placental insufficiency, the fetus experiences chronic low oxygen levels and reduced nutrient supply, including lower blood sugar and disrupted amino acid transfer. This is the leading cause of fetal growth restriction, and both early- and late-onset growth restriction are significant risk factors for cerebral palsy.
The fetal brain has a built-in defense mechanism sometimes called “brain sparing,” where blood flow is redirected to prioritize the brain when oxygen runs low. This works for a while, but if the oxygen deprivation continues, the system eventually fails. The combination of prolonged low oxygen, low blood sugar, oxidative stress, and inflammation damages developing brain tissue. Placental abruption, where the placenta partially or fully separates from the uterine wall before delivery, can cause a more sudden and severe loss of oxygen with similar consequences.
Maternal Infections That Cross to the Fetus
A group of infections collectively known as TORCH infections pose a serious threat to fetal brain development. The acronym covers toxoplasmosis, rubella, cytomegalovirus (CMV), and herpes simplex virus. Because the fetal immune system is still immature, the baby can’t fight these infections effectively on its own. The result can be problems with brain growth and organ development, including microcephaly (an abnormally small head).
Children affected by TORCH infections may not show obvious symptoms at birth but can develop vision loss, hearing loss, seizures, and learning disabilities after age two. CMV is particularly common and is one of the leading infectious causes of neurological damage before birth. Rubella, while now rare in countries with widespread vaccination, remains a risk in parts of the world without routine immunization.
Inflammation and Infection of the Fetal Membranes
Chorioamnionitis, an infection of the membranes surrounding the fetus, triggers a cascade of inflammation that can damage the developing brain even when the infection itself doesn’t reach the baby directly. The mechanism works through inflammatory signaling molecules called cytokines. When the placenta becomes inflamed, the fetus mounts its own inflammatory response, and these cytokines are toxic to fragile developing brain tissue.
This inflammatory pathway is one of the two major causes of a specific type of brain injury called white matter damage, which is most common between 23 and 30 weeks of gestation. At that stage, the cells responsible for insulating nerve fibers in the brain are especially vulnerable to inflammation, oxidative stress, and toxic byproducts of the immune response. White matter damage is strongly linked to cerebral palsy, particularly the spastic forms that affect movement and muscle tone.
Fetal Stroke
A stroke can happen before birth when a blood clot blocks blood flow to part of the fetal brain or when a blood vessel ruptures. Maternal conditions that raise the risk include high blood pressure disorders of pregnancy (gestational hypertension, preeclampsia) and blood clotting disorders that make clot formation more likely. Ischemic strokes, caused by blocked blood flow, occur at a rate of roughly 18 per 100,000 births.
Fetal strokes often go undetected until after birth, when a baby shows signs of weakness or abnormal movement on one side of the body. The resulting brain damage depends on where the stroke occurs and how much tissue is affected, but it frequently leads to a form of cerebral palsy that primarily involves one side.
Multiple Pregnancies
Carrying twins, triplets, or more significantly increases the risk of cerebral palsy. European population data show that multiples develop cerebral palsy at a rate of about 7 per 1,000 live births, compared to 1.6 per 1,000 for singletons. That translates to a risk roughly four times higher.
Several factors drive this increased risk. Multiple pregnancies are more likely to result in preterm birth, low birth weight, and placental insufficiency. Twins who share a placenta face additional dangers, including unequal blood flow between them. If one twin dies in the womb, the surviving twin faces a sharply elevated risk of brain injury from sudden changes in blood pressure and circulation.
Genetic Mutations
Not all prenatal cerebral palsy stems from oxygen loss or infection. In some cases, spontaneous genetic mutations (ones neither parent carries) disrupt normal brain development before birth. These de novo mutations can affect how brain cells migrate, how nerve fibers form, or how the brain’s white matter develops. Some mutations cause structural brain abnormalities visible on imaging, such as clusters of misplaced brain cells that failed to migrate to their correct position during development.
Researchers have also identified overlap between genes linked to cerebral palsy and those that cause hereditary spastic paraplegia, a group of conditions that affect nerve fibers controlling leg movement. This genetic overlap helps explain why some children diagnosed with cerebral palsy have no identifiable pregnancy complication, birth injury, or infection. Their brain developed differently because of its genetic blueprint.
Maternal Thyroid Disorders
Thyroid problems during pregnancy can affect fetal brain development because the baby depends on maternal thyroid hormones, especially in early pregnancy before the fetal thyroid starts functioning. A population-based study found that thyroid disorders identified during pregnancy were associated with roughly three times the odds of the child developing unilateral spastic cerebral palsy, the type affecting one side of the body.
Severe iodine deficiency provides the clearest evidence of this link. In regions where iodine deficiency is endemic, children born to affected mothers have a substantial risk of impaired motor and cognitive function. Brain imaging in these children shows patterns consistent with cerebral palsy. In countries with iodine-fortified salt, this cause is rare, but other thyroid conditions can still pose a risk if untreated during pregnancy.
Blood Type Incompatibility
When a mother’s blood type is incompatible with her baby’s, her immune system can produce antibodies that attack the baby’s red blood cells. The most well-known form is Rh incompatibility, but ABO incompatibility and other red blood cell antibody mismatches also contribute. The destruction of red blood cells floods the newborn’s system with bilirubin, the yellow pigment that causes jaundice.
Most newborn jaundice is harmless, but extremely high bilirubin levels can stain and damage specific brain structures, particularly areas that control movement. This condition, called kernicterus, results in a severe form of cerebral palsy characterized by involuntary writhing movements and abnormal postures. Kernicterus is considered one of the few fully preventable causes of cerebral palsy. Routine prenatal blood typing, preventive injections for Rh-negative mothers, and monitoring of newborn bilirubin levels have dramatically reduced its occurrence, though cases still happen when screening or treatment is delayed.
How Multiple Causes Overlap
In practice, cerebral palsy during pregnancy rarely comes down to a single cause. A fetus experiencing placental insufficiency may also be exposed to inflammation. A genetically vulnerable brain may be less resilient to a brief drop in oxygen that a typical fetus would tolerate without damage. Prematurity, which is itself a consequence of many of these risk factors, adds another layer of vulnerability because the brain’s blood vessels and insulating cells are not yet mature enough to withstand stress.
This overlap is one reason why identifying the cause of a specific child’s cerebral palsy can be challenging. In many cases, it involves a combination of predisposing factors and triggering events rather than one clear moment of injury.