Cerebral Palsy

A disorder of tone, movement or posture from an early, static (non-progressive) insult to the brain — an umbrella term for a clinical syndrome, not a single diagnostic entity. The most common physical/movement disorder in childhood, affecting 1.5–2.5 per 1000 live births; more than 37,000 Australians live with CP. A lifelong condition — while the underlying brain change is non-progressive, associated musculoskeletal changes tend to worsen over time and need regular monitoring/intervention. Disability severity spans a large spectrum, from no activity restriction to profound multi-system impairment.

Cause and risk factors

Cause is usually multifactorial/unclear (no identifiable risk factor is found in many children — its absence should not prevent further investigation/ management), but the underlying insult is grouped by timing:

• Prenatal (≈80% of cases): congenital brain malformations, intrauterine infection (CMV, rubella, other early-pregnancy viral illness), intrauterine stroke, chromosomal abnormalities, maternal or infant thrombophilia, Rh/ABO incompatibility, chorioamnionitis, placental insufficiency/abnormal placental pathology, multiple gestation.
• Perinatal: hypoxic-ischaemic insults/prolonged intrapartum hypoxia, CNS infection, stroke, kernicterus/severe neonatal jaundice.
• Postnatal (≈10% of cases): accidental or non-accidental head trauma, CNS infection or encephalitis, stroke, anoxic insult, complex congenital heart disease, other severe illness before birth or in the first 2 years of life.

Prematurity is the single biggest risk factor, and risk rises as gestational age falls: a French cohort found cerebral palsy in 6.9% of infants born at 24–26 weeks and 4.3% of those born at 27–31 weeks, against a much lower rate beyond 32 weeks. Grade 3–4 intraventricular haemorrhage and necrotising enterocolitis both increase risk further, and a low arterial cord pH roughly doubles it. Low birth weight compounds the same risk — 5–15% of infants under 1500g develop CP.

Antenatal prevention

A Cochrane overview of 15 systematic reviews (27 RCTs, 32,490 children) found high-quality evidence that antenatal magnesium sulphate before preterm birth reduces the risk of cerebral palsy in the surviving child — the one intervention shown clearly effective for prevention. By contrast, antibiotics given for preterm labour with intact membranes, and immediate delivery for suspected fetal compromise, were both associated with a higher rate of cerebral palsy (moderate-quality evidence) — the opposite of what was intended. Repeat courses of antenatal corticosteroids (beyond a single course) showed no clear difference in cerebral palsy risk.

Common comorbidities: epilepsy, vision/hearing impairment, learning difficulties/intellectual impairment, speech difficulties, dental decay, feeding difficulties/poor nutrition, constipation, incontinence, sleep problems.

Definition (5 key elements)

1. An umbrella term for a group of disorders.
2. Permanent, but not unchanging.
3. A disorder of movement and/or posture and motor function.
4. Due to a non-progressive interference, lesion or abnormality…
5. …originating in the immature brain.

Classification

Multiple systems are used:

• Severity: mild (no activity restriction, mobile without aids); moderate (needs assistance/aids); severe (wheelchair, marked restriction). The Gross Motor Function Classification System (GMFCS) is the standard 5-level functional scale used by specialist services.
• Topography: paresis (weakened) vs plegia (paralysed); mono- (1 limb), di- (2, usually legs), hemi- (arm + leg, same side), para- (lower body), quadri- (4 limbs), penta- (4 limbs + head/neck/breathing).
• Motor function/tone: spastic diplegic (legs affected more than arms), spastic hemiplegic (one side, arms usually more than legs), spastic quadriplegic (all 4 limbs, often upper limbs worse), dyskinetic/hyperkinetic (choreoathetoid — rapid, dance-like contractions plus slow writhing), dystonic (sustained, twisting involuntary contractions), or ataxic (unsteady, incoordinated, hypotonic).

Other descriptive terms in use: hypertonic/hypotonic, athetoid. See also gait abnormalities for the scissoring/spastic diplegic gait pattern typical of spastic CP, including its role in early recognition and orthotic/surgical referral.

Physical signs and diagnosis

Average age at diagnosis is 18 months, though many signs are present earlier: low muscle tone (“floppy” on picking up); poor head/trunk control; feeding/swallowing difficulty; hypertonia, muscle spasm or limb stiffness; unusual movements (writhing, dystonia, athetosis, chorea); abnormal postures (extensor posturing of head/neck, leg scissoring); diminished or exaggerated deep tendon reflexes; primitive reflexes (Moro, atonic neck reflex) persisting beyond 6 months; unilateral neglect or clear hand preference before 18 months; asymmetric weakness; delayed development (not sitting/rolling by 6 months, not walking by 15–18 months, not speaking simple phrases by 24 months).

Cerebral palsy remains a clinical diagnosis from history and examination — imaging or testing is not required to make the diagnosis; the specialist you refer to can arrange investigations if indicated. When they are, brain MRI is the preferred modality (86–89% sensitivity for the underlying abnormal neuroanatomy, better anatomical detail than CT); a neonatal/early-infancy cranial ultrasound can identify intraventricular haemorrhage, ventriculomegaly and periventricular leukomalacia. Standardised tools aid early detection before a confident clinical diagnosis is possible: the General Movements Assessment (infants <5 months — absent fidgety movements between 9–20 corrected months has 98% sensitivity) and the Hammersmith Infant Neurological Examination (2–24 months, 90% sensitivity).

Consider an alternative diagnosis (metabolic, genetic or a slowly progressive disorder rather than CP) when there is: no risk factor for CP, developmental regression, hypotonia with true weakness, rapid loss of skills or worsening with fasting/illness, oculomotor abnormalities, or sensory loss — several of these have specific treatments and should not be missed under a default CP label.

Management

Early intervention

If CP is suspected in an infant/toddler, arrange early intervention as soon as possible for assessment and diagnosis — earlier intervention is linked to improved outcomes.

• ≤20 weeks: urgent referral for a general movements assessment.
• >20 weeks: refer to both a medical specialist and allied health assessment (e.g. a hospital cerebral palsy clinic — physio/speech/OT).
• >2 years: screening hip X-rays with the referral — progressive hip displacement (subluxation/dislocation) is the most common musculoskeletal complication of CP, usually arising in childhood/adolescence.

Spasticity and tone management

Spasticity is the most common motor disturbance in CP and typically worsens over childhood, affecting at least one limb. Botulinum toxin type A (BoNT-A) is considered first-line treatment for focal lower-limb spasticity. A Cochrane review of 31 trials (1,508 children) found moderate-quality evidence that BoNT-A improves gait pattern, joint range of motion and treatment satisfaction compared with placebo, with a similar rate of side effects to placebo; benefit compared with usual care/physiotherapy alone was only very-low-quality evidence. BoNT-A performed similarly to a series of below-knee plaster casts, and better than leg splints for joint range of motion. Other options for tone include oral agents (baclofen, benzodiazepines, dantrolene, tizanidine), trihexyphenidyl/gabapentin for dystonia, and — for refractory spasticity — an intrathecal baclofen pump, selective dorsal rhizotomy, or orthopaedic surgery (tendon release, hip derotation, spinal fusion).

Ongoing GP role

Motor/posture management is largely led by therapists and specialist clinics, often with multiple team members, where the GP takes a coordinating role. GPMP/TCA and routine health surveillance should cover all health domains: annual health assessment, vaccinations, cancer screening, hearing/vision screening, prompt specialist referral for each issue that arises. Family planning should be discussed as the patient grows.

Other GP responsibilities:

• Facilitating access to funding streams and services (encourage NDIS enrolment)
• Diet and growth monitoring
• Bladder issues, including UTIs
• Constipation management
• Pressure sore care
• Sleep issues
• Behavioural support
• Pain management
• Family issues — parental coping, sibling dynamics
• Routine paediatric care (immunisations, common infections/injuries) — these may present special challenges depending on CP type/severity

Parent education matters — families need to understand the likely cognitive/communication issues ahead and how to seek support (NDIS for GPs factsheet).

Complications and prognosis

Complications are common and should be actively screened for rather than waiting for the patient/family to raise them: pain (50–75%), intellectual disability (50%), epilepsy (25–45%), speech impairment (40–50%), strabismus (50%), hip subluxation/dislocation (30%), urologic conditions such as incontinence/neurogenic bladder (30–60%), hearing impairment (10–20%), sleep disturbance (23%), blindness (10%), and — in moderate–severely affected patients — osteopenia (77%). Aspiration pneumonia is the most common cause of early death in severely affected patients.

Motor prognosis depends on CP subtype and early developmental milestones. Children who go on to walk independently typically do so by age 3; those who walk with support may take up to age 9. A child not walking by age 9 is unlikely to walk with support. Good prognostic signs for independent walking include sitting by 24 months and crawling by 30 months; poor signs include no head control by 20 months, retained primitive reflexes, no postural reflexes by 24 months, and not crawling by 5 years. Most children with CP survive into adulthood; severely affected patients have reduced life expectancy.