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This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
Key points
- Non-progressive brain lesion causing permanent motor impairment — but functional consequences evolve as child grows
- Prevalence ~2 per 1,000 live births. Most common cause of physical disability in childhood
- Subtypes: spastic (70–80% — unilateral/bilateral), dyskinetic (10–15%), ataxic (5–10%), mixed
- Causes: most often antenatal (80%) — prematurity/PVL, HIE, congenital malformation, infection, stroke. Only 10% due to birth asphyxia
- Red flags: abnormal tone (increased or decreased), persistent primitive reflexes, hand preference before 12 months, delayed motor milestones
- Management: MDT — physiotherapy, OT, SALT, orthotics, botulinum toxin for focal spasticity, baclofen, orthopaedic surgery. Manage comorbidities: epilepsy (30%), learning disability, visual/hearing impairment, GORD, drooling
Overview
Cerebral palsy is an umbrella term for a group of permanent disorders of movement and posture attributed to non-progressive disturbances in the developing fetal or infant brain. While the brain lesion itself is static, the clinical manifestations evolve as the child grows. The motor disorders are often accompanied by disturbances of sensation, perception, cognition, communication, behaviour, and epilepsy. Classification is based on motor type (spastic, dyskinetic, ataxic) and topographical distribution (unilateral or bilateral).
Epidemiology
Cerebral palsy affects approximately 2 per 1,000 live births in the UK. It is more common in preterm infants (up to 100 per 1,000 in extremely preterm). The majority of cases (80%) have antenatal causes. Periventricular leukomalacia (PVL) is the most common pathology in preterm infants (leading to spastic diplegia). Hypoxic-ischaemic encephalopathy at term accounts for approximately 10%. Male:female ratio is approximately 1.3:1.
Clinical Features
Symptoms
Delayed motor milestones — late sitting, late walking, or not achieving walking
Early hand preference before 12 months (suggests contralateral hemiplegia)
Stiffness or floppiness (abnormal tone)
Feeding difficulties, drooling, swallowing problems
Seizures (develop in ~30%)
Signs
Spasticity: increased tone, velocity-dependent (clasp-knife), hyperreflexia, clonus, extensor plantar responses
Dyskinesia: involuntary, uncontrolled, recurring movements (choreoathetoid, dystonic)
Ataxia: unsteady gait, intention tremor, poor coordination
Persistent primitive reflexes beyond normal age (Moro, ATNR, palmar grasp)
Scissoring of legs (adductor spasticity), toe-walking
Investigations
First-line
Clinical diagnosisBased on motor abnormalities, developmental history, and exclusion of progressive conditions
MRI brainRecommended in all children with CP — identifies aetiology in 80–90% (PVL, basal ganglia lesions, malformations, stroke)
Second-line
General Movements Assessment (GMA)Prechtl GMA at 3–5 months (fidgety movements) — highly predictive of CP if absent fidgety movements. Enables early diagnosis
GMFCS (Gross Motor Function Classification System)Levels I–V classifying gross motor function — guides prognosis and intervention planning
Specialist
Genetic testingConsider if no MRI abnormality, family history, or dysmorphic features — some genetic mimics of CP (DOPA-responsive dystonia, hereditary spastic paraplegia)
Metabolic screenIf progressive course or atypical features — exclude treatable metabolic conditions
1
Multidisciplinary team
- Physiotherapy — stretching, strengthening, mobility aids, postural management
- Occupational therapy — fine motor skills, adaptive equipment, seating
- Speech and language therapy — communication, feeding and swallowing
- Orthotics — AFOs, splints to prevent contractures
- Orthopaedic surveillance — hip surveillance programme (hip displacement risk in GMFCS III–V)
2
Spasticity management
- Botulinum toxin A: focal spasticity — injected into specific muscles (e.g. gastrocnemius for equinus)
- Oral baclofen or diazepam: generalised spasticity
- Intrathecal baclofen pump: severe generalised spasticity in GMFCS IV–V
- Selective dorsal rhizotomy (SDR): NICE-approved for ambulant children with spastic diplegia (GMFCS II–III)
3
Comorbidity management
- Epilepsy (~30%): standard AED management per NG217
- GORD: very common — PPI or alginate, fundoplication if severe
- Feeding difficulties: dietetic input, gastrostomy if unsafe swallow or inadequate nutrition
- Pain management: musculoskeletal pain is common and underrecognised
- Behavioural and emotional support: ADHD, anxiety, depression common
Complications
- Hip displacement: Progressive subluxation/dislocation in GMFCS III–V — hip surveillance programme essential
- Contractures and scoliosis: From spasticity and immobility
- Aspiration pneumonia: From oromotor dysfunction and GORD
- Chronic pain: Musculoskeletal — often undertreated
- Osteoporosis: Non-weight-bearing, anticonvulsants, poor nutrition
UKMLA Exam Tips
- 1Hand preference before 12 months is abnormal — suggests contralateral hemiplegia (cerebral palsy)
- 2PVL (periventricular leukomalacia) in preterm infants causes spastic diplegia (legs > arms)
- 3Basal ganglia injury (e.g. acute profound hypoxia at term) causes dyskinetic CP
- 4CP is NON-PROGRESSIVE — if symptoms are progressive, reconsider the diagnosis (neurodegeneration, metabolic)
- 5GMFCS I–V: I = walks without restrictions, V = transported in wheelchair, severely limited self-mobility
- 6Absent fidgety movements on General Movements Assessment at 3–5 months is the earliest reliable predictor
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