Cerebral palsy (CP) is a complex neurodevelopmental disorder primarily caused by brain injury or abnormal brain development that affects movement and posture. There is substantial evidence linking **neglected or adverse prenatal conditions**—such as infections, inflammation, placental abnormalities, and maternal health issues—to the risk of cerebral palsy, although the relationship is multifactorial and not solely dependent on prenatal factors.
One key prenatal contributor to cerebral palsy is **inflammation in the placenta and fetal brain**. The placenta acts as a critical interface between mother and fetus, and inflammation here can trigger a cascade of immune responses that harm the developing brain. Research shows that placental inflammation can impair myelin formation (the protective sheath around nerve fibers), cause neuroinflammation, and disrupt brain structure and function, all of which can lead to long-term neurodevelopmental disorders including cerebral palsy[1]. Various prenatal exposures—such as infections (e.g., Ureaplasma parvum), opioid or cannabis exposure, and other inflammatory triggers—alter the placental microenvironment, increasing the risk of brain injury in the fetus[1][2].
**Infections during pregnancy** are a significant prenatal risk factor. Some infections may be silent but still cause damage to the fetal brain, especially if they lead to preterm birth. For example, Ureaplasma parvum infection is common but often overlooked; certain strains of this infection are more damaging to white matter development in the fetal brain, which is crucial for motor control. This damage can increase the risk of cerebral palsy and other neurodevelopmental delays[2]. Preterm birth itself, often a consequence of infection or inflammation, is a major risk factor for cerebral palsy because the immature brain is more vulnerable to injury[2][6].
**Maternal health conditions**, such as hypertensive disorders during pregnancy, have also been studied for their impact on fetal brain development. A large meta-analysis involving over 29 million children found that hypertensive disorders were associated with increased risks of autism spectrum disorder, ADHD, intellectual disability, and developmental delays. However, this study did not find a direct increased risk of cerebral palsy linked to maternal hypertension after adjusting for factors like gestational age and birthweight[3]. This suggests that some prenatal conditions may contribute indirectly to cerebral palsy risk by increasing preterm birth or low birthweight, which themselves are risk factors for brain injury.
The types of brain injury leading to cerebral palsy often originate prenatally or perinatally and include:
– **Hypoxic-ischemic encephalopathy (HIE):** Brain damage caused by reduced oxygen and blood flow, often during labor or delivery, but prenatal factors can predispose to this condition[4].
– **Periventricular leukomalacia (PVL):** Damage to the white matter near the brain’s ventricles due to reduced blood and oxygen flow, strongly linked to cerebral palsy[4].
– **Intracranial hemorrhage:** Bleeding in the brain, sometimes caused by maternal infections or placental complications, which can occur prenatally or during birth[4].
– **Cerebral dysgenesis:** Abnormal brain development during pregnancy, sometimes influenced by infections or genetic factors, increasing cerebral palsy risk[4].
Neglected prenatal care or unrecognized prenatal conditions can exacerbate these risks. For example, inadequate monitoring of infections or maternal health issues ma
