Cerebral palsy

Cerebral palsy is a group of permanent disorders of movement and posture caused by a non-progressive injury or maldevelopment of the fetal or infant brain. The brain lesion does not worsen over time, but clinical manifestations change as the child grows, and many children have associated sensory, cognitive, communication, behavioural, and epilepsy-related comorbidities.

The core mechanism is an acquired disturbance of the developing brain in the antenatal, perinatal, or early postnatal period. Injury to corticospinal pathways (primary motor cortex/white matter) produces upper motor neuron features and spasticity; basal ganglia/deep grey matter injury is linked to dyskinetic phenotypes; cerebellar pathway involvement contributes to ataxia. MRI patterns in cohorts commonly include white matter injury (especially in preterm infants), basal ganglia/deep grey matter lesions, congenital malformations, and focal infarcts. Although the lesion is static, secondary musculoskeletal changes (contracture, hip displacement, scoliosis, pain) evolve over time. See Figure from standard paediatric neuroimaging texts showing periventricular white matter injury and basal ganglia injury patterns.

• Prematurity (risk rises as gestational age falls)
• Low birth weight, especially very low/extremely low birth weight
• Multiple gestation (twins/triplets/higher-order multiples)
• Maternal infection, including chorioamnionitis and severe antenatal genitourinary/respiratory infection
• Congenital infection (TORCH)
• Placental abruption and other placental vascular/thrombotic pathology
• Perinatal hypoxic-ischaemic encephalopathy (accounts for a minority of cases)
• Intraventricular haemorrhage and neonatal encephalopathy
• Neonatal sepsis, especially in very low birth weight infants
• Severe neonatal hyperbilirubinaemia
• Postnatal CNS infection (for example meningitis) or significant head injury before age 3 years
• Fetal genetic/metabolic disorders and congenital brain malformations
• Maternal teratogen exposure (for example warfarin)

• Feeding difficulty and undernutrition/poor growth
• Aspiration and recurrent chest infections
• Gastro-oesophageal reflux and vomiting
• Chronic constipation
• Drooling/sialorrhoea with skin and social impact
• Hip subluxation/dislocation, contractures, scoliosis, and chronic musculoskeletal pain
• Low bone mineral density/osteopenia/osteoporosis and fracture risk
• Epilepsy
• Visual and hearing impairment
• Learning disability and communication disorders
• Behavioural, emotional, and mental health disorders
• Sleep disturbance including sleep-disordered breathing
• Pressure ulcers in severe immobility
• Reduced quality of life and, in severe multisystem disease, reduced life expectancy

Outcome is highly heterogeneous and depends on motor severity, cognition, communication ability, epilepsy control, and burden of comorbidity. The lesion itself is non-progressive, but functional needs typically change with growth, requiring ongoing reassessment. Early functional markers are useful in exams: children who can sit by age 2 years are more likely to walk by age 6 years than those who cannot sit or roll. Most people survive into older adulthood, but severe impairment (especially with major swallowing dysfunction and high care needs) is associated with shorter life expectancy.