Cerebral palsy (CP) describes a group of permanent disorders affecting the development of movement and posture, resulting in activity limitations. The condition is caused by a non-progressive disturbance that occurred in the developing fetal or infant brain. Historically, CP was often attributed solely to birth trauma or oxygen deprivation during delivery, but modern research shows this accounts for only a small percentage of cases. Current scientific understanding is that CP rarely stems from a single factor. Instead, it results from a complex interplay between acquired—or environmental—factors and a child’s underlying genetic vulnerability.
Acquired Causes During Development and Birth
The non-genetic, or acquired, factors leading to CP involve any event that causes damage to the brain before, during, or shortly after birth, a period when the brain is still rapidly developing. The single largest acquired risk factor is being born prematurely, especially before the 32nd week of pregnancy, or having a low birth weight, defined as less than 5 pounds, 8 ounces. Premature birth makes the white matter of the brain, which transmits signals throughout the body, particularly susceptible to injury between 26 and 34 weeks of gestation.
Maternal infections during pregnancy can also trigger an inflammatory response that damages the fetal brain. Infections such as rubella, cytomegalovirus (CMV), and toxoplasmosis can cross the placenta, leading to abnormal brain development. The body’s inflammatory response to these infections is thought to release proteins that can harm the developing neural tissue.
Issues around the time of delivery, known as perinatal problems, represent another group of acquired causes. These issues include a lack of oxygen to the brain, or asphyxia, which can occur if the umbilical cord is compromised or the placenta detaches prematurely. Severe bleeding in the brain, often due to a fetal stroke where a blood vessel is blocked or ruptures, also interrupts the blood flow needed for healthy brain development.
In the period immediately following birth, severe neonatal jaundice can pose a risk if not treated promptly. Jaundice is caused by high levels of bilirubin, and in extreme cases, this can lead to a type of brain damage called kernicterus, which can cause athetoid CP. Less commonly, CP can be acquired after the first month of life through external events like serious infections, such as meningitis, or through head trauma.
Genetic Predisposition and Inherited Risk
While CP has long been viewed as purely a result of environmental or acquired factors, recent large-scale genomic studies confirm that genetics play a significant role in a substantial minority of cases. Researchers have identified specific gene mutations that can directly cause CP by disrupting the formation and wiring of brain circuitry during early development. These direct genetic causes are often rare, single-gene mutations that can arise spontaneously, meaning they are not inherited from either parent.
In some cases, the causal mutations are inherited from parents who do not have the condition themselves, suggesting a recessive inheritance pattern. Studies sequencing the DNA of children with CP have found that a causative or likely causative genetic variant is present in up to one-quarter of patients. This figure is particularly high for children with no known acquired risk factors like prematurity or infection.
Beyond direct causation, a genetic predisposition involves inheriting a combination of genes that make a person’s brain more vulnerable to injury from external events. This inherited risk explains the phenomenon of familial recurrence, where the risk for subsequent children in a family is slightly increased even without a clear environmental cause. Certain genetic variations may increase a child’s susceptibility to developing complications from an infection or being born prematurely, thus setting the stage for CP.
How Genes and Environment Interact
The most common explanation for CP is that it is a multifactorial condition, arising from the complex interaction between a child’s genetic makeup and external environmental factors. In this scenario, a child may inherit a genetic vulnerability that makes their developing brain subtly more fragile or susceptible to damage. This vulnerability alone may not cause CP, but it lowers the threshold for an acquired event to result in permanent injury.
For example, a genetic change might predispose an infant to have a slightly less robust immune response or a more sensitive vascular system in the brain. If this genetically vulnerable infant then experiences a relatively mild acquired stressor, such as a minor maternal infection or a premature birth, the combination results in the brain damage associated with CP.
This interaction fundamentally shifts the focus from solely blaming birth trauma to recognizing underlying developmental issues that make the brain vulnerable to otherwise minor stressors. Research now suggests that a genetic factor can contribute to known risk factors, such as making a baby more likely to be born prematurely, which then exposes the developing brain to greater risk. Understanding this interplay moves the diagnosis beyond a search for a single, obvious cause toward a more personalized understanding of a child’s unique biological risk profile.