Cerebral Palsy
A non-progressive disorder of movement and posture caused by injury to the developing brain.
Overview
Cerebral palsy affects ~1 in 400 UK children. Classified by motor pattern (spastic, dyskinetic, ataxic, mixed), distribution (uni-/bilateral) and functional level (GMFCS I–V). Most have associated comorbidities — epilepsy, learning disability, communication, feeding, visual, hearing problems — that shape long-term care.
Symptoms
- • Delayed motor milestones, persistent primitive reflexes
- • Increased or fluctuating muscle tone, scissoring
- • Asymmetric hand use before 1 year
- • Feeding difficulties, drooling
- • Associated: seizures, learning, vision, speech difficulty
Risk factors
- • Prematurity (<32 weeks), low birth weight
- • Multiple pregnancy
- • Chorioamnionitis, placental abnormality
- • Birth asphyxia
Causes
- • Antenatal (~75%): congenital malformation, intrauterine infection, stroke, genetic
- • Perinatal: hypoxic-ischaemic encephalopathy, kernicterus
- • Postnatal (<2 years): meningitis, head injury, near-drowning
🚨 Red flags — seek urgent care
- • Loss of skills — suggests progressive disorder, not CP
- • New-onset seizures, signs of raised intracranial pressure
- • Aspiration pneumonia in a child with feeding difficulty
- • Hip displacement (Reimer's >30%)
When to seek care
- • Concerns about motor development at any check
- • Difficulty with feeding, swallowing or growth
- • Loss of previously acquired skills
Diagnosis
- • Clinical: persistent motor disorder by 2 years (often by 6–12 months in severe cases)
- • MRI brain (preferred over CT) — identifies aetiology in ~80%
- • Genetic and metabolic testing if MRI normal or atypical features
- • Functional assessment: GMFCS, MACS, CFCS
- • Hearing, vision, swallowing and hip surveillance from diagnosis
Treatment
- • Multidisciplinary care: paediatrician, physiotherapy, occupational therapy, speech and language, dietetics, orthotics
- • Spasticity: oral baclofen, botulinum toxin, intrathecal baclofen, selective dorsal rhizotomy
- • Orthopaedic surgery for fixed deformity, dislocated hip, scoliosis
- • AAC for communication; specialist seating and mobility
- • Manage comorbidities: epilepsy, GORD, constipation, sleep, pain
- • Hip surveillance programme (annual X-ray for higher GMFCS)
Prevention
- • Antenatal corticosteroids and magnesium sulfate for preterm labour (neuroprotection)
- • Therapeutic hypothermia for moderate-severe HIE
- • Prompt treatment of neonatal jaundice and infection
Complications
- • Hip displacement and dislocation
- • Scoliosis, contractures
- • Aspiration, malnutrition, osteoporosis
- • Epilepsy, depression, chronic pain
- • Reduced life expectancy in severe disability
Prognosis
Wide variability. Most children with GMFCS I–II have normal life expectancy and walk independently. Severe involvement carries greater medical risk and shortened life expectancy.
Education & self-care
Early, coordinated multidisciplinary care, hip surveillance and targeted spasticity treatment maximise independence and prevent avoidable complications.
Frequently asked questions
Is cerebral palsy progressive?
The brain injury is fixed, but musculoskeletal effects (contractures, hip displacement) progress without surveillance and therapy.
Can my child walk?
Depends on GMFCS level — most at level I–II walk independently; level III with aids; IV–V use wheeled mobility.
Is genetic testing useful?
Yes — 25% of children diagnosed clinically with CP have a genetic disorder that can change management or family counselling.