Cerebral palsy

• Cerebral palsy (CP) is a group of permanent disorders of movement, muscle tone and posture caused by non-progressive injury to the developing fetal or infant brain.^[3]
• It is the most common physical disability of childhood, with a prevalence of 1.5 to 3 per 1,000 live births, and about half of affected children are born at term with no identified risk factor.^[3]
• The motor type is classified as spastic (diplegic, hemiplegic, quadriplegic), dyskinetic (extrapyramidal), ataxic, or mixed.^[3]
• Severity of gross motor limitation is graded on the five-level GMFCS, from walking without limitation to being transported in a wheelchair.^[4]
• Management is multidisciplinary and life-long: physiotherapy, postural care, tone-reducing medicines and focal botulinum toxin, orthopaedic surgery when needed, and surveillance of hips, nutrition and seizures.^[1][2]

By the end of this page you should be able to:

1. Define cerebral palsy and explain why the brain lesion is non-progressive while the clinical picture can change and worsen with growth.
2. List the main risk factors and typical timing of the brain injury for each motor type.
3. Classify a child by motor type and by GMFCS level.
4. Recognise early motor signs and red flags that should prompt referral or re-investigation.
5. Describe the common comorbidities and their approximate frequency.
6. Outline the multidisciplinary management pathway, from early therapy to botulinum toxin, baclofen and orthopaedic surgery.
7. Say what surveillance is needed and what to do in a low-resource setting.

Cerebral palsy is a clinical description, not a single disease with one cause. It names a motor disorder that results when a developing brain is injured at any point from early gestation to about the first two years of life, roughly until brain maturation is largely complete. The injury itself does not progress, but the growing skeleton, muscles and nervous system change around it, so a young person's function can deteriorate in adolescence even though the lesion is static. Because the brain, the whole nervous system, and everyday activities are all affected at once, good care of CP is team care that follows the person from infancy into adult life.^[1][3]

The most useful way to think about CP for a first-time reader is cause, timing, and distribution: where the brain was injured, when it happened, and which body regions are involved. Those three determine the motor type, the likely comorbidities, and the plan. A preterm infant with periventricular white matter injury typically has spastic diplegia; a term infant who had a hypoxic-ischaemic encephalopathy tends to have dyskinetic CP; a focal arterial stroke in utero or around birth produces spastic hemiplegia. None of these can be diagnosed from imaging alone; imaging describes the lesion, while the diagnosis is clinical.^[1][3]

Four facts in this definition do most of the clinical work:

• Permanent. The motor disorder is lifelong. There is no cure, although function can be improved.
• Non-progressive. The underlying brain lesion does not worsen with time. New deterioration in a child labelled CP should make you stop and ask whether something else is going on (see red flags below).
• Developing brain. The injury occurred before the brain finished maturing. That is what separates CP from adult stroke or head injury, and it is why the motor pattern can look different at age two from age ten.
• Accompanied by. CP is not only moving badly. Epilepsy, sensory and cognitive problems, feeding and hip problems are part of the same spectrum rather than separate surprises.^[1][3]

CP is classified by the predominant motor pattern, and by the body regions involved. The categories in the table below are used together in practice, for example spastic diplegia, GMFCS level III. The percentages are those reported by Patel et al. and reflect older clinical series; local cohorts vary.^[3]

Spasticity is by far the most common tone pattern, followed by dyskinesia, hypotonia and ataxia.^[3] The distinction between tone types matters not only for prognosis but for treatment: selective dorsal rhizotomy helps spasticity, not dystonia, and dystonia may respond to oral baclofen or trihexyphenidyl instead.^[2]

Motor type does not tell you what a child can actually do. For that the Gross Motor Function Classification System (GMFCS), a five-level scale, grades gross motor function, especially walking, for ages 2 to 18. It is age-related, so the same child is classified differently at 18 months and at 12 years, and it is not a diagnosis alone: classify once the motor pattern has settled.^[4][2] NICE summarises it as level I walks without restrictions, II walks without assistive devices, III walks with assistive devices, IV has limited self-mobility, and V has severely limited self-mobility even with assistive devices.^[2]

Three companion scales are commonly used alongside GMFCS and together give a clearer picture than topography alone: the Manual Ability Classification System (MACS) for use of the hands, the Communication Function Classification System (CFCS) for everyday communication, and the Eating and Drinking Ability Classification System (EDACS) for feeding safety. Together these four scales standardise how children with CP are described across a multidisciplinary team.^[4]

CP has an incidence of 2 to 3 per 1,000 live births across the world, with variation between high-income, low- and middle-income countries, and geographic region. Reported prevalence is higher in infancy because abnormal neuromotor findings often resolve over the first two to five years of life. Post-neonatal CP, arising from brain injury after the neonatal period and before 5 years of age, is recognised; the most common causes are traumatic brain injury, near-drowning and meningitis.^[3]

The group is heterogeneous. Being born early or small is the biggest single risk, yet many other factors are linked with CP, and about half of children who develop CP were born at term with normal birth weight and no identified risk factor.^[3]

CP comes from a non-progressive disturbance of the developing brain. The timing rather than the final diagnosis drives the classification:

• in preterm infants, intracerebral haemorrhage and periventricular leukomalacia are the main lesions, and most injuries sit in the window before 34 weeks of gestation;
• in term infants, hypoxic-ischaemic injury, kernicterus, maternal-fetal infection and arterial stroke predominate;
• after 5 years of age, a motor disorder is usually not classified as CP.^[3]

NICE lists the following as independent risk factors and groups them by timing.^[1]

• Antenatal: preterm birth, with risk rising as gestational age falls; chorioamnionitis; maternal respiratory tract or genito-urinary infection treated in hospital.
• Perinatal: low birth weight; chorioamnionitis; neonatal encephalopathy; neonatal sepsis (especially with a birth weight under 1.5 kg); maternal respiratory tract or genito-urinary infection treated in hospital. ^[1]
• Postnatal: meningitis.

Additional factors reported by Patel et al. include congenital brain malformation, genetic susceptibility, hypoxic-ischaemic encephalopathy, in-utero or perinatal stroke, assisted reproduction, kernicterus, maternal clotting disorders, multiple gestation, neonatal seizures or sepsis, post-neonatal meningitis or traumatic brain injury, and pre-pregnancy obesity.^[3]

Risk factors interact and accumulate. NICE notes that independent risk factors can have a cumulative impact on the developing brain and may act at any stage. On MRI, brain abnormality patterns in children with CP are reported at approximate prevalences of white matter damage 45%, basal ganglia or deep grey matter damage 13%, congenital malformation 10%, and focal infarcts 7%. White matter damage is more common in children born preterm and in spastic than dyskinetic CP, whereas basal ganglia or deep grey matter injury is mostly associated with the dyskinetic subtype. Congenital malformations as a cause are more common at term and are associated with higher levels of impairment.^[1]

Two risk factors deserve emphasis because they are, in part, preventable:

• Neonatal encephalopathy can follow sepsis or hypoxic-ischaemic injury or both. In children with CP born after 35 weeks, encephalopathy attributed to perinatal hypoxic-ischaemic injury is reported in around 20% and not attributed to such injury in around 12%. Where CP is associated with a perinatal hypoxic-ischaemic injury, severity of long-term impairment is often related to the severity of the initial encephalopathy, and the dyskinetic motor subtype is more common than other subtypes.^[1]
• Kernicterus, the result of unconjugated bilirubin crossing the blood-brain barrier in severe neonatal jaundice, typically produces choreoathetotic or dystonic CP, with gaze and hearing abnormalities, and remains a major cause of dyskinetic CP in settings with delayed recognition.^[3]

Where CP occurs after the neonatal period, approximate prevalences reported by NICE are meningitis 20%, other infections 30% and head injury 12%. Because these are post-neonatal injuries, prevention, emergency management and rehabilitation follow ordinary first principles of acute care rather than antenatal obstetrics.^[1]

The core lesson is that nothing about the movement disorder is arbitrary. CP is an upper motor neuron problem: injury to the developing corticospinal and basal ganglia circuits removes normal inhibition of stretch reflexes, producing spasticity, dystonia and weakness together, and the pattern reflects where the brain was injured.

• Spastic diplegia follows periventricular leukomalacia in the late second and early third trimester, injuring oligodendrocyte precursors and the corticospinal fibres that pass beside the lateral ventricles. Because arm fibres are more medial and better myelinated at that age, the legs take the brunt. Most of these children have normal cognition.^[3]
• Dyskinetic CP follows deep grey matter and basal ganglia injury, most often from prolonged hypoxia-ischaemia or kernicterus in a term infant. The motor deficit is therefore combined with extrapyramidal circuit dysfunction rather than isolated corticospinal loss. These children have a higher rate of dysphagia, seizures, hearing and visual impairment.^[3]
• Spastic hemiplegia from an arterial stroke is a regional injury; cognition and the contralateral arm and hand often dominate the disability.^[3]
• Ataxic CP comes from cerebellar or posterior fossa injury and presents with hypotonia and balance difficulty.^[3]

Because the brain injury is static, the clinical course is about what grows around it. Persistent primitive reflexes (see below) block normal motor sequences, muscles shorten into contractures against fast-growing bones, and joints deform in children who are not weight-bearing. Secondary problems such as hip migration and scoliosis therefore appear years after birth and are the main targets of surveillance.^[1][3]

CP is suspected when a parent, carer or professional notices that a baby's tone, posture or movement is not right, or that milestones are late or asymmetric. Risk factors, birth and perinatal events, hospital admissions, and family history all belong in the history, and their absence is itself a red flag. Listen also for feeding fatigue, poor head control in early infancy, asymmetric use of the hands, or paucity of movement on one side.^[1][3]

Persistence of primitive reflexes or primary motor patterns beyond the expected age is a key clinical characteristic of CP. These reflexes, normal in the newborn, should integrate as the brain matures; failure to integrate prevents the sequential acquisition of higher-level motor skills.^[3] NICE lists early motor abnormalities that should trigger referral, including unusual fidgety movements, asymmetry or paucity of movement, abnormal tone (hypotonia, spasticity or dystonia), late head control, rolling and crawling, and feeding difficulties.^[1]

Common early signs in infancy also include head lag beyond early months, scissoring of the legs when lifted, rigidity or floppiness, arching of the back, and one-handed reaching while the other hand stays fisted.^[3]

The most common delayed motor milestones in CP, as listed by NICE, are not sitting by 8 months (corrected for gestational age), not walking by 18 months (corrected for gestational age), and early asymmetry of hand function (hand preference) before 1 year (corrected for gestational age).^[1] A child who has not reached the sitting milestone at 8 months needs assessment and not reassurance; the same is true for any persistent hand preference before the first birthday, because it often signals hemiplegia before weakness becomes obvious.^[1][3]

NICE also recommends referral for persistent toe walking, and an enhanced follow-up programme for at-risk infants up to 2 years corrected age.^[1]

Examination should look beyond a list of reflexes:

• Tone assessed at rest and with passive movement, in the arms, legs, trunk, and around the mouth; spasticity is velocity-dependent and varies with arousal.
• Distribution and severity of the motor pattern; a single limb's involvement suggests stroke rather than generalised injury.
• Primitive and postural reactions: persistence beyond the age expected for each (Moro, tonic neck, grasping, and a foot asymmetry) supports the diagnosis; absence of expected antigravity responses is also informative.
• Orthopaedic screen: hip range (loss of abduction is an early warning of hip displacement), foot posture, and spinal alignment.
• Functional state: how the child moves, feeds, communicates and plays in real life; classification scales belong alongside, not instead of, clinical findings.^[1][2][3]

Red flags for disorders other than CP should make you pause or seek a specialist: no known risk factors, a family history of a progressive neurological condition, loss of skills already acquired, unexpected focal neurological signs, or MRI findings suggestive of or out of keeping with a static injury. Discussing uncertainty openly with parents is part of the diagnosis.^[1]

CP is diagnosed clinically after other causes have been considered. Disorders that can look like CP but are progressive or treatable include hereditary spastic paraplegias, neurometabolic and neurogenetic conditions, muscular dystrophies, spinal muscular atrophy, and post-injury states. The practical separators are clinical: absence of risk factors, loss of previously attained abilities, focal or unexpected neurological signs, a deteriorating rather than plateauing course, and imaging that does not match the clinical picture. NICE recommends review of the diagnosis whenever development does not follow expected patterns, and referral to paediatric neurology when red flags are present.^[1]

Where a diagnosis of CP cannot yet be made, the label "high risk of cerebral palsy" allows CP-specific interventions to be started while follow-up continues. This approach is based on systematic reviews reported by Patel et al., in which a combination of clinical history, neuroimaging, and standardised tools (for infants under 6 months corrected age, the Prechtl General Movements Assessment, the Hammersmith Infant Neurological Examination, and term-age MRI) identify risk, while for infants 6 months and older MRI, the Hammersmith examination and structured developmental assessment are used.^[3]

MRI of the brain is recommended to establish aetiology where it is not clear from history, development and examination, and is abnormal in around 90% of children with CP.^[3] It may show white matter loss, periventricular leukomalacia, brain malformation, focal infarct, or deep grey matter injury, and it supports classification and genetic or metabolic counselling when needed. Repeat imaging is worth considering if the clinical course changes or red flags appear. MRI alone is not reliable for predicting prognosis.^[1][3]

No blood test diagnoses CP. Genetic, neurometabolic or chromosomal testing is indicated when red flags are present or the aetiology is uncertain, particularly when a treatable condition is possible. Cranial ultrasound has a role in preterm infants but does not exclude later periventricular injury. Early, accurate diagnosis relies on the combination of history, standardised tools and imaging rather than any single investigation.^[1][3]

Hip displacement is a mechanical consequence of non-weight-bearing muscle imbalance, not part of the original brain injury, and is silent until late. NICE CG145 recommends offering a hip X-ray if there are clinical concerns or at 24 months in bilateral CP, and repeating it annually in children at GMFCS level III, IV or V. Clinical indicators of displacement include pain arising from the hip, a clinically important leg length difference, worsening hip abduction or range, increasing tone, deteriorating sitting or standing, and increasing difficulty with hygiene. A migration percentage above 30% is the threshold at which closer monitoring (X-ray after 6 months, then every 6 months if displacement is increasing by more than 10 percentage points per year) and orthopaedic review are considered.^[2]

Baseline ophthalmological and orthoptic assessment is recommended at diagnosis, with regular hearing assessment, because about one in two children with CP has some form of visual impairment (cerebral visual impairment in around one in five) and about one in ten has hearing impairment. Nutritional status, growth, eating and drinking safety, and pain should be reviewed at every contact.^[1]

There is no single positive test for CP. Diagnosis rests on three pillars: a non-progressive motor disorder characteristic of a disturbance of the developing brain, present from early infancy, together with a compatible history and examination. The pattern often evolves during the first years, so a diagnosis made before 2 years should be revisited if the expected course is not seen.^[1][3]

Severity and staging are functional rather than pathologic. The GMFCS describes gross motor function, MACS hand use, CFCS communication, and EDACS eating and drinking safety, and together they give the functional profile that drives management and prognosis. MRI adds aetiological category but not a stage. These tools are complementary to each other and to clinical judgement, not replacements for it.^[4]

In the short term, NICE gives parents three commonly discussed prognostic markers for walking: if the child can sit at 2 years of age it is likely, although not certain, that they will walk unaided by age 6; if they cannot sit but can roll at 2 years, walking unaided is possible; if they cannot sit or roll at 2, unaided walking is unlikely.^[1]

Management follows the least invasive option first, stepped up only when goals are not met, and every plan is individualised and agreed with the young person and parents. Core features are an early multidisciplinary assessment through a child development service, a network of care with defined pathways, treatment goals in the WHO International Classification of Functioning domains, and regular review of programmes. Physiotherapy is the backbone; medicines and surgery are adjuncts to it, never replacements.^[1][2]

Physiotherapy and occupational therapy should be offered promptly and tailored to individual goals such as skill, function and participation, prevention of contracture and pain. Programmes that start by age 4 to 5 are relatively more effective than those started later. Components include 24-hour postural management, task-focused active-use therapy such as constraint-induced movement therapy followed by bimanual therapy, muscle strengthening, and integration into daily activities. After botulinum toxin, intrathecal baclofen, orthopaedic surgery or selective dorsal rhizotomy, an adapted physical therapy programme is an essential part of management rather than an option.^[2][3]

Orthoses, equipment and assistive technology (ankle-foot orthoses, seating, standers used for function rather than solely bone density, wheelchairs, augmentative communication devices) are selected against individual goals, with attention to fit, skin, hygiene, and the views of the child and family. Physiotherapy evidence for improving strength, range of movement and endurance in CP is well summarised by Patel et al.^[2][3]

Oral drugs are considered when spasticity contributes to discomfort or pain, muscle spasms or functional limitation. Diazepam is useful when a rapid effect is needed, such as a pain crisis, and is given as a bedtime dose initially. Baclofen is chosen when a sustained long-term effect is desired; treatment starts with a low dose and increases stepwise over about 4 weeks to obtain the best effect, with reduction in stages when stopping to avoid withdrawal. If one drug used for 4 to 6 weeks is unsatisfactory, combined diazepam and baclofen is considered; adverse effects such as drowsiness are managed by reducing or stopping the drug.^[2]

The guideline also advises caution using diazepam or baclofen in children with poorly controlled epilepsy, respiratory compromise or increased risk of aspiration, and checking these risks before postural and motor programmes are started.^[2]

Botulinum toxin type A (BoNT-A) is considered for focal spasticity that impedes gross or fine motor function, compromises care or hygiene, causes pain, disturbs sleep, or prevents tolerance of orthoses. It is used in focal lower limb spasticity, frequently for dynamic equinus foot deformity, and in hemiplegic upper limb spasticity. Effectiveness is best between 1 and 6 years of age for lower extremity spasticity and 5 to 15 years for spastic hemiplegia, and the intervention is best provided by clinicians within the network team with expertise in child neurology and musculoskeletal anatomy. Injections are guided by ultrasound or electrical stimulation when appropriate; ultrasound-guided injection of salivary glands is also used for drooling, but only as a specialist option after anticholinergics and with specific licensed products, because high doses can cause swallowing difficulty.^[2][3]

Safety teaching before BoNT-A must be specific: rare but serious complications, swallowing or breathing difficulties, can occur at any time during the first week after injection, and the family must return to hospital immediately if they occur. An adapted physiotherapy programme is essential afterwards, and response is reviewed 6 to 12 weeks after injections. Units of different BoNT-A products are not interchangeable, so licensed indications and doses for the individual product must be used.^[2]

Continuous pump-administered intrathecal baclofen is considered when non-invasive treatment leaves spasticity or dystonia causing pain or spasms, postural or functional difficulty, or problems with self-care, especially in children at GMFCS level III, IV or V with bilateral spasticity. Contraindications include being too small to accommodate the pump, intercurrent infection, uncontrolled epilepsy and respiratory disorders at risk of failure; an intrathecal baclofen test is performed before implantation and the pump is implanted within 3 months of a satisfactory response. Oral baclofen for dystonia in CP is off-label in children. Families need verbal and written information on pump management, possible withdrawal and when to seek help.^{[2] [3]}

Selective dorsal rhizotomy is considered to improve walking in children at GMFCS level II or III with spasticity, by a trained multidisciplinary team, with full discussion of irreversibility and uncertain long-term outcomes.^[2]

Orthopaedic surgery is an established adjunct in CP. Timely surgery can prevent deterioration and improve function. Indications include concern or radiological evidence of hip displacement (migration percentage above 30%, or migration increasing by more than 10 percentage points per year), spinal deformity, and limitation of limb function by muscle shortening, contractures or bony deformities. Many procedures are best done as single-event multilevel surgery, with a planned programme of adapted physiotherapy, orthoses and any tone-reducing treatment afterwards.^[2][3]

The common orthopaedic problems in CP are summarised from Patel et al. in the table below and reflect what a physiotherapy and surgical service must be ready to manage: equinus and rotational deformities, hip displacement or dislocation, avascular and pain problems, and scoliosis or kyphosis.^[3]

Ongoing monitoring includes tone, contractures, hip displacement, nutritional status and growth, bone health, communication, pain and sleep; low bone mineral density is a risk in non-ambulant children. Families should be included in decisions, and plans should contain a clear route to a specialist pain team when pain is unexplained. Transfer to adult services needs preparation and a named transition process.^[1]

The comorbidities are not incidental: they determine quality of life and survival and they follow the severity of the motor and cognitive impairment. NICE gives the following approximate frequencies, which should be quoted to families without overstating precision.^[1]

Other problems recorded in the literature and summarised by Patel et al. include pulmonary problems such as recurrent aspiration and restrictive lung disease, genitourinary problems, skin ulceration, dental malocclusion, sleep disturbance, delayed or precocious puberty, attention deficit hyperactivity disorder, depression and self-injurious behaviour, and pain from multiple sources (hip, muscle, scoliosis, reflux, constipation).^[3] Because CP affects both body systems and participation, its impact on the child shows up across the whole assessment, which is why repeated review across the first years of life is much more useful than a single assessment.^[1][3]

Among the comorbidity set, the two to stress to students are nutritional and epileptic: feeding difficulty is common, and NICE describes a pathway of clinical and specialist assessment, postural adjustment, texture modification and enteral feeding when oral intake is still inadequate; around one third of children need antiepileptic treatment, more often in dyskinetic CP. Dyskinetic movements must not be mislabelled as seizures.^[1]

Most children with CP survive to adult life. Overall survival of all children with CP until age 20 is 90%; 95% of those with diplegia and 75% of those with quadriplegia survive until age 30, and 95% of children with mild cognitive deficit and 65% of those with severe cognitive deficit survive until age 38. Two out of three individuals with CP are ambulatory with or without assistance, three out of four can speak, and one out of two have normal cognitive abilities, with appropriate support and intervention.^[3]

The severity of physical, functional or cognitive impairment drives both life expectancy and function: learning disability is more common with GMFCS III to V, and epilepsy and hip problems accumulate with severity. The goal of care is therefore not only to preserve walking but to keep the young person as healthy, participatory and comfortable as possible across a long life, into middle adulthood where health-service continuity can be challenging.^[1][3]

Primary prevention targets the antenatal and perinatal causes:

• prevention of preterm birth and low birth weight;
• antenatal magnesium sulphate if preterm birth is imminent before 32 weeks of gestation, which is neuroprotective and reduces the risk of CP; ^[3]
• therapeutic hypothermia in term and late preterm infants with hypoxic-ischaemic encephalopathy, initiated within 6 hours of birth, lowering body or head temperature by 2 °C for 48 hours.^[3]

Secondary prevention relies on enhanced follow-up of at-risk infants up to 2 years corrected age, use of predictive tools such as the General Movements Assessment under 5 months and the Hammersmith Infant Neurological Examination, MRI where aetiology is unclear, and early referral so that CP-specific interventions can start early under the hypothesis of neuroplasticity.^[1][3]

Screening and surveillance in practice include hip X-rays at the threshold described above, baseline ophthalmology and orthoptics at diagnosis and repeating visual and hearing assessment, regular hearing screens, nutritional review, pain and sleep review, and surveillance of low bone mineral density in non-ambulant children using dietary assessment and laboratory testing (calcium, phosphate, alkaline phosphatase, vitamin D and a spot urinary calcium to creatinine ratio if indicated).^[1]

• Preterm infants. These children carry a high burden of periventricular white matter injury and spastic diplegia. Follow-up is enhanced and early diagnosis made in at-risk programmes. Cranial ultrasound identifies some but not all of the relevant injury, and MRI may be needed before 2 years of age.^[1][3]
• Term infants after hypoxic-ischaemic encephalopathy. Dyskinetic CP is more common, with oral-motor and feeding problems, hearing loss and epilepsy. The initial encephalopathy severity predicts long-term impairment. Therapeutic hypothermia is the proven preventive measure.^[1][3]
• Post-neonatal CP. Management follows prevention of brain injury, emergency care of infection, trauma and drowning, then rehabilitation on ordinary principles.^[1][3]
• Non-ambulant children. Need the most intensive support for feeding, hip surveillance, bone health, pressure area care and powered mobility, but many go on to productive adult lives with good support.^[1][3]
• Young adults. Transition to adult services, employment, relationships, contraception and fertility counselling, and continuity of orthopaedic and tone management are essential and often under-provided.^[1]

The diagnosis and much of the management of CP depend more on clinical skill than on expensive technology:

• A general clinical examination and a single anteroposterior hip X-ray detect most problems a first contact clinician needs to act on; learn to examine hip abduction and to refer on the CG145 clinical indicators.^[2]
• Physiotherapy, postural management, adaptive equipment and task-specific active-use therapy can be delivered by trained therapists, nurses and parents, as early as possible and by daily activities a family can sustain.^[2][3]
• When botulinum toxin is unavailable or unlicensed, treat focal spasticity with oral diazepam or baclofen according to cautions, and with physiotherapy and orthoses.^[2]
• When intrathecal pumps and selective dorsal rhizotomy cannot be provided, refer early to a regional centre before deformities become fixed.^[2]
• Surgery for hip displacement needs paediatric orthopaedic expertise; refer early because late displacement is harder to salvage.^[2][3]
• Families need information about the condition in terms they can use, including expected developmental progress and the availability of local support.^[1]
• Where antenatal care is limited, progress in antenatal steroid, maternal infection control and facility-based delivery matters as much as neonatal resuscitation.^[3]

Plain text only (no links in this version): hypoxic-ischaemic encephalopathy in the newborn; prematurity and neonatal care; neonatal jaundice and kernicterus; epilepsy in childhood; hearing and visual impairment in children; nutrition support and enteral feeding; low bone density in childhood; selective dorsal rhizotomy; single-event multilevel orthopaedic surgery.