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Cerebral palsy
Allan Colver, Charles Fairhurst, Peter O D Pharoah
Lancet 2014; 383: 1240–49
Published Online
November 20, 2013
Institute of Health and Society,
Newcastle University, Royal
Victoria Infirmary, Newcastle
upon Tyne, UK
(Prof A Colver FRCPCH);
Department of Paediatric
Neurosciences, Evelina
Children’s Hospital, Guy’s and
Saint Thomas’ NHS Foundation
Trust, London, UK
(C Fairhurst FRCPCH); and
University of Liverpool,
Liverpool, UK
(Prof P O D Pharoah FRCP)
Correspondence to:
Prof Peter O D Pharoah,
University of Liverpool,
Liverpool L69 3GB, UK

The syndrome of cerebral palsy encompasses a large group of childhood movement and posture disorders. Severity,
patterns of motor involvement, and associated impairments such as those of communication, intellectual ability, and
epilepsy vary widely. Overall prevalence has remained stable in the past 40 years at 2–3·5 cases per 1000 livebirths,
despite changes in antenatal and perinatal care. The few studies available from developing countries suggest
prevalence of comparable magnitude. Cerebral palsy is a lifelong disorder; approaches to intervention, whether at an
individual or environmental level, should recognise that quality of life and social participation throughout life are
what individuals with cerebral palsy seek, not improved physical function for its own sake. In the past few years, the
cerebral palsy community has learned that the evidence of benefit for the numerous drugs, surgery, and therapies
used over previous decades is weak. Improved understanding of the role of multiple gestation in pathogenesis, of
gene environment interaction, and how to influence brain plasticity could yield significant advances in treatment of
the disorder. Reduction in the prevalence of post-neonatal cerebral palsy, especially in developing countries, should be
possible through improved nutrition, infection control, and accident prevention.

In cerebral palsy’s milder forms, individuals present
with mild spasticity and contracture in one arm and leg
on one side of the body, which interferes with fluid
movement and fine manual dexterity. The individual
might have some sensory inattention to that side of the
body and to that visual field, and might have focal
epilepsy. At the other end of the spectrum, an individual
can present with involvement of the four limbs, with a
mixed picture of spasticity and dyskinesia. The individual
can have substantial contractures and scoliosis, and
therefore require a wheelchair for mobility. They might
also have associated severe learning difficulties, cortical
visual impairment, and be prone to chest infections.
Cerebral palsy is a syndrome of motor impairment that
results from a lesion occurring in the developing brain;
the disorder varies in the timing of the lesion, the clinical
presentation, and the site and severity of the impairments.
The earliest description of the disorder is attributed to
the orthopaedic surgeon William Little in 1862.1 Several
attempts to define and classify the syndrome have been
made. Recently, the International Executive Committee
for the Definition of Cerebral Palsy, proposed the
following definition: “Cerebral palsy describes a group of
permanent disorders of the development of movement
and posture, causing activity limitation, that are attributed to non-progressive disturbances that occurred in the
developing fetal or infant brain. The motor disorders of
cerebral palsy are often accompanied by disturbances of
sensation, perception, cognition, communication and
behaviour, by epilepsy, and by secondary musculoskeletal
problems”. This definition is supplemented by a full
explanation of the terms used in the definition.2

Search strategy and selection criteria
References included in this Seminar were identified by the
authors based on their respective areas of expertise and
supplemented by unsystematic database searches.


The complexity of the syndrome is clear from its various
classifications; cerebral palsy can be defined according to
the anatomical site of the brain lesion (cerebral cortex,
pyramidal tract, extrapyramidal system, or cerebellum);
clinical symptoms and signs (spasticity, dyskinesia [dystonic and choreo-athetotic forms], or ataxia); topographical
involvement of extremities (diplegia, quadriplegia, or
hemiplegia); timing of presumed insult (prepartum,
intrapartum, or postneonatal); and classification of degree
of muscle tone (isotonic, hypotonic, or hypertonic).3
Standard classifications are essential for research and
transfer of knowledge. The 9th and 10th International
Classifications of Disease include many categories of
cerebral palsy and substantial inconsistency exists in
how clinicians interpret these guidelines.4 A
straightforward classification is needed that can be
applied reliably by clinicians and used in registers. Such
a classification (with categories of unilateral spastic,
bilateral spastic, dyskinetic, and ataxic) and an associated
decision tree was developed by the Surveillance of
Cerebral Palsy in Europe (European network SCPE) and
is now widely adopted.5

Development of registers for cerebral palsy, with an
emphasis on a shared definition of the syndrome and
efforts to ensure complete identification of cases, has
shown a cerebral palsy prevalence of 2·0–3·5 per 1000 livebirths.6–9 Prevalence in developing countries seems to be
similar, but data sources are not well established.10,11
Cerebral palsy prevalence is inversely associated with
gestational age and birthweight, with a prevalence
ranging from 90 cases per 1000 neonatal survivors
weighing less than 1000 g to 1·5 cases per 1000 for those
born weighing 2500 g or more.12–14 The upper age limit
used for definition of postneonatal cerebral palsy is
arbitrary, but in most studies it is considered to be about
5 years. About 10% of all cases of cerebral palsy are
classified as postneonatal,15 which are largely attributable
to CNS infections such as meningoencephalitis and head
www.thelancet.com Vol 383 April 5, 2014

For example. and the UK. infant death of one twin is associated with a significant increase in risk of cerebral palsy in the survivor. was confirmed in an Australian cohort. low birthweight. this twin could be the cause of cerebral palsy in some singleton births. in the second trimester. hypoglycaemia. marriage between close family members is not common. 70 60 50 40 30 20 10 0 1981 1982 1983 1984 1985 1986 1987 1988 1989 1990 1991 1992 1993 1994 1995 Midpoint birth year Figure 1: Prevalence of cerebral palsy in infants with birthweights of 1000–1499 g from nine European countries in birth years 1980–96 (3 year moving average) Countries are Denmark.36 In developed countries. the high rates of cerebral palsy observed in preterm births occur when gestational birthweight deviates from this optimum (figure 2). This problem can be split into two parts: first. iodine deficiency causes a specific type of cerebral palsy.16 1241 . France. In some developing countries.28 Neonatal asphyxia was thought to be a key cause of brain damage in preterm or term babies. insults during the first trimester are associated with www. However. with periventricular white matter damage. the increasing proportion of multiple births of decreasing birthweights.21 Most pregnancies are monochorionic (where twins share the same amniotic sac). nature. However.20.35 therefore. causes of cerebral palsy are routinely prevented and can go unnoticed.16 and a decrease. which then levelled out.31. For every gestation and for each type of cerebral palsy.17 As noted more than a century ago by Sigmund Freud. the inverse association of the prevalence of cerebral palsy with birthweight and.33 Although these theories do not seem to help to explain cerebral palsy in singletons or dichorionic multiple pregnancies. Population studies suggest a 50–100 times increase in the prevalence of cerebral palsy in a live cotwin of a stillbirth20–23 compared with singleton pregnancies.com Vol 383 April 5. and often referred only to the need for administration of oxygen after birth. mothers receive prompt treatment for rhesus isoimmunisation (in which severe jaundice is an established cause of dyskinetic cerebral palsy). Ireland. and neonatal infections. emergency caesarean section. Prevalence of cerebral palsy in infants of normal birthweight (≥2500 g) seems not to have changed over time. birth asphyxia. Reproduced from Platt and colleagues. Embolic theory proposes that the transference of thromboplastin or thromboemboli from the dead fetus to the cotwin leads to cerebral damage. with cortical and deep grey matter damage.25 A systematic review26 done in 2013 reported ten risk factors as significantly associated with cerebral palsy: placental abnormalities. 2014 cerebral maldevelopments such as schizencephaly. In general. there is a one in 56 probability that one infant has cerebral palsy and a one in 430 probability that both have cerebral palsy. an optimum birthweight exists. major and minor birth defects. comparisons of the risk of cerebral palsy in singleton and multiple births are confounded by the effect of birthweight and gestational age. Compared with singletons.30 Monochorionicity can have an important role in the pathogenesis of cerebral palsy because the vascular anastomoses in the placenta serve both fetuses and transfusion potentially could occur between fetuses. When both twins are livebirths. Most cases of cerebral palsy result from an interference in brain development in utero and MRI scanning has helped understanding of these processes.37 A controlled trial of iodinated oil 100 90 80 Prevelence per 1000 livebirths injuries (accidental and non-accidental). and timing of the definitive cerebral insult. respiratory distress syndrome. meconium aspiration.24 A risk factor is not necessarily causal and other recently identified risk factors have yielded little in the way of preventive strategies. and many immunisations are directed at prevention of infant infections such as meningitis.19 When both twins are livebirths.thelancet. and in the third trimester.32 ischaemic theory suggests that some exsanguination occurs from the surviving fetus into the low resistance dead fetus. which is a known risk factor for cerebral palsy22 even in very preterm infants. The Netherlands. neonatal seizures. adverse factors might have been present for some time during pregnancy. second.27 This optimum birthweight effect is especially pronounced when fetal assessment of weights in the womb are used to generate weight standards rather than actual weights of delivered babies. Sweden. Italy.34. obstetric ultrasound has shown that one or more embryos from a multiple conception can be lost early in pregnancy as a vanishing twin or triplet. the evidence for asphyxia was applied loosely. The cerebral palsy risk in a same-sex survivor with infant death of the cotwin is 167 per 1000 compared with 21 per 1000 in an unlike pair. the relative risk of cerebral palsy in twins is 5·6 and in triplets is 12·6.Seminar Pathogenesis Although many mechanisms have been proposed to explain the cause. Asphyxia is now thought to account for 10–20% of cerebral palsy cases29 and attribution of causation now requires evidence of encephalopathy.18 multiple pregnancy is also a risk factor for cerebral palsy.14 but a decreasing prevalence in low birthweight infants has been noted in Europe (figure 1). Germany. Norway.

cerebral palsy was cited in 28%. however. nonambulant. an increased risk was reported. are reported to not be predictive of cerebral palsy. enhanced identification and treatment of such infections has not been effective.com Vol 383 April 5.52 An abnormal scan finding is not a prerequisite for diagnosis of cerebral palsy but scans are recommended to assist clinical management. provided supplementation was given before conception. If all impairment domains are not severe. which is a particular problem in those with additional severe cerebral palsy. 1242 About 85% of children with cerebral palsy have an abnormal MRI scan. and metabolic disorders that can mimic cerebral palsy. doparesponsive dystonias. In individuals with mild to moderate impairment.51 Fetal standard Number per 1000 livebirths 1000 MRI 100 10 1 0·1 –3 –2 –1 0 <28 weeks 28–31 weeks 1 2 3 –3 Z score 32–36 weeks 37–38 weeks –2 –1 0 1 2 3 39–41 weeks >42 weeks Figure 2: Prevalence of cerebral palsy by Z score of weight for gestation Reproduced from Jarvis and colleagues. partially sighted. UK. ambulatory.40 To date.54–56 If severe impairments are present. a normal scan can suggest the need for a more detailed investigation of some genetic conditions such as hereditary spastic paraplegias. Coventry. The severities of mental.Seminar Conventional standard attention deficit disorder. and 27% to 40 years (JL Hutton. A UK report57 noted that in adults with severe intellectual impairment. personal communication).54 Of individuals with cerebral palsy in the UK who were alive at age 2 years with four severe impairments (intelligence quotient <50. withdrawal of a rich source of dietary iodine precipitated an epidemic of cerebral palsy. accidents in 18%. Life expectancy To estimate life expectancy. complete genome and exome sequencing will probably identify genes and combinations of genes that are predictive of cerebral palsy.50 However. When studies linking anonymised national datasets have been possible. although this observation might be because more children with severe impairments (who used to die before diagnosis of cerebral palsy could be made) are now more likely to live at least into their early years. Several studies have reported chorioamnionitis to be a risk factor for cerebral palsy. including isolated bilateral polymicrogyria and spastic types in closely related families. Next was pneumonia at 23% and aspiration at 11%. 34% to 30 years. but was largely attributable to increased risk of multiple pregnancies and preterm births. Life expectancy does not seem to be improving. then life expectancy is reduced approximately in proportion to the number and severity of associated impairments. survival is only marginally less than that of individuals without cerebral palsy.39 Maternal infections such as rubella and cytomegalovirus can result in cerebral palsy. 72% lived to 10 years. especially clotting abnormalities such as factor V Leiden. 44% to 20 years.49. but transfusion problems between fetuses might also provide a unified pathogenic mechanism in some cases. A significant increase in the prevalence of non-cerebral congenital anomalies coexistent with cerebral palsy has been reported. especially when cerebral palsy is stated as the only cause of death. features of severe physical illness might not have been noticed.60 interpretation of information in death certificates is difficult. and poor manual function). Several single gene Mendelian disorders cause cerebral palsy.48 Genetic factors are increasingly implicated in our understanding of cerebral palsy. Artificial reproductive therapies could play a part in the genesis of cerebral palsy. University of Warwick. The most common cause in individuals with severe cerebral palsy was cerebral palsy in 50% of cases. although these associations are difficult to study because of strict confidentiality regulations in most countries.59. quality of care can also be relevant. An MRI scan can provide an estimate of the timing of the lesion and assist in determination of whether the lesion is responsible for the motor impairment or is an incidental finding. 2014 .38 In another study. a register of all cases is needed with dates of birth and regular updates of deaths to allow actuarial analysis. and pneumonia in 12% of www. manual. especially in preterm babies. Finally. some cases of cerebral palsy that have a fetal origin associated with non-cerebral congenital anomalies42–46 have a genetic or teratogenic cause.53 Findings could provide families with a more complete explanation of the cause of their child’s cerebral palsy or could show lesions such as bilateral polymicrogyria with implications for genetic counselling. as in previous studies. intellectual impairment. and visual impairments are significant factors in survival.thelancet. and many of these genes could be shared with predictors of other neurodevelopmental disorders such as autism.47. and epilepsy. However.27 established that the disease could be prevented. The most recent study to report cause of death in individuals with cerebral palsy in Australia58 noted that. Single nucleotide polymorphisms.41–43 Undoubtedly. cardiac causes in 15%.

2014 neurological disorders such as cerebral palsy. including pain.67.com Vol 383 April 5. pain relief.65. and activity restrictions inevitably score lower in individuals with a health disorder such as cerebral palsy.80. Alternatively. children and young people are asked to complete questionnaires as well as parents. for children and young people.70 A life-course perspective also highlights the transition phase. as well as the adoption of a more realistic approach to what physical rehabilitation might achieve. a recent book has set out the different questionnaires that are available to measure the constructs.86 However. Furthermore.66 Fatigue. Rather than seeking small improvements in physical function during childhood which are then lost.71–73 Paediatric services often fail to prepare young people for adult health care. thereby rendering the brain less adaptive. and employment. gastrostomy tubes.61 The ICF recognises three constructs: body structure and function.67.81 and in proportion to the severity and number of impairments. education. activity limitation. Outcomes are also poor in this period.74–76 and is either not recognised or poorly managed by clinicians. However. when a young person’s health care transfers from child to adult services at the same time as they progress from adolescence to adulthood. Such factors could have little influence on an individual’s overall subjective wellbeing. and the ICF recognises two further constructs: environmental and personal factors. but little evidence exists on which to choose. stretching does not produce clinically significant changes in contractures or function. Inclusion of cerebral palsy on death certificates as a secondary rather than the sole cause of death would benefit knowledge about cause of death and how to consider prevention.92. parents can manage and set boundaries differently for a disabled child.93 Such difficulties can be due to disruption of neural pathways or networks that regulate emotions and behaviour. and participation.79 The ICF defines participation as involvement in life situations and is captured across nine domains including self-care. Therapy combined with medical and surgical interventions offers benefit. Seeking normalisation of physical impairment in childhood only achieves gains in the direction of normalisation. Pain in children and adults with cerebral palsy is much more common than previously thought. interpersonal relationships. therapy is painful for many children. Each construct can influence the others. thereby allowing child behaviour that parents would not allow in a typically developing child.64. whereas children usually have less control over such choices.Seminar reported cases. most research regards it as a paediatric illness.64 Adults with cerebral palsy have disadvantages in social life and employment. in individuals with www. This shift is in line with the United Nations Declaration on the Rights of the Child63 that emphasises the need to listen to and take into account children’s views. pain.68 and some evidence suggests that physical ageing might occur more rapidly than in adults without the disorder. and employment. Quality of life In the past decade.82–84 Health-related quality of life of individuals with cerebral palsy is lower than that of the general population. frequency of treatment. Many physical therapies are available. In those who are able to self-report. Furthermore. subjective wellbeing is broadly similar to that of the general population according to quantitative (figure 3)87–89 and qualitative studies. Recognition that outcomes in adulthood have been less than positive has shown the need for clinical practice to adopt a lifelong perspective on the disorder.94 Improving outcomes As the ICF and life-course frameworks predict.69. a divergence exists between trying to make the body of the individual to function more normally and accepting the person as they are and concentrating on environmental adjustments. the constructs captured such as services needed. as children enter adolescence.90. and depressive symptoms are also common in adults with cerebral palsy. studies of individuals with cerebral palsy have been done within the framework of the International Classification of Functioning. Participation is consistently reduced in children and adults with cerebral palsy compared with the general population. such independence should be encouraged rather than restricted by parents and clinicians.thelancet. including spasms. their interactions are influenced by the context in which an individual lives. Means to measure ICF concepts have been developed or revised. and hypersensitivity around operative scars. Moreover. contractures.85. Although cerebral palsy is a lifelong disorder. schooling.62 Increasingly.95 1243 . little evidence exists in favour of the benefit of postural management but substantial evidence of its disadvantages.91 Children with cerebral palsy have more psychological difficulties than do children of the general population.77 which is of concern because. hip dislocation. gastric reflux. there is not a causative progression from an impairment of structure to participation. Societal views and preconceptions of the parents can mix with parental feelings of guilt and sadness to fundamentally change how parents deal with a child with cerebral palsy.78 Moreover. even these might not be sustained beyond the few months of a trial or are lost as an individual grows heavier. Disability and Health (ICF). at least in the short term. an adult is able to balance choices between therapy.76 Assisted stretching has been identified as the daily activity most frequently associated with pain. Pain in individuals with cerebral palsy is caused by many reasons. concentration on communication and technical skills needed for the workplace might be more important. Adults with cerebral palsy state that their participation in life does not depend on being able to walk but on communication and being able to manage and control their environment.

not growth itself. The social model of disability. 2014 .kidscreen. interquartile range. The importance of family-centred services for disabled children. The most common disorders are strabismus. but also because of development of appropriate measures of functional ability that allow goals for clinical www. Various factors. However. especially when an individual is on anticonvulsants and has nutritional difficulties.101 In patients with severe bilateral involvement. mostly attributable to cortical visual impairment. poor nutrition and growth. family lifestyle effects child participation as much for disabled as for able-bodied children (eg.104 Osteopenia and osteoporosis are recognised in non-ambulant adults with cerebral palsy. all interventions must be planned. or hypermetropia. and bowel motility. especially after surgery to correct severe scoliosis. About 35% of children with cerebral palsy have a visual problem17 and therefore. be free of stress. Permanent sensorineural deafness is less common and. and endocrine and gastrointestinal problems can contribute to poor growth and nutrition in individuals with cerebral palsy.96 These differences suggest that environmental adjustments might be possible. many environmental adjustments can also be delivered locally. striking differences exist in participation between individuals from different countries or different regions of the same country. This change is due.102 Unsafe swallowing and aspiration can require gastrostomy. and adjacent values are shown.105 Poor nutrition can lead to immune dysfunction106 and immobility. Moreover. it minimises the effect of medical difficulties while maximising physical ability. high rates of infection. and poor hearing and vision. environmental adjustment.100 in which problems in participation are attributed to failure of society to accept 1244 and adapt to the needs of the individual. First. if present. absorption. has been emphasised. and better able to be responsive to their child. can be as high as 10%.87 For more on KIDSCREEN see http://www. some of which will need legislation or regulation to raise a country to the standards of those that best facilitate participation. and a balance needs to be reached for each individual between growth and the complexity and invasiveness of any intervention. and deformity can lead to skin and urinary tract infections. in part. visual field defect. About 8% of children with cerebral palsy have severe visual impairment. is usually associated with neonatal gentamicin therapy or neonatal hyperbilirubinemia. diagnostic difficulties can also arise if the underlying movement disorder mimics epileptic events. and constipation are frequently reported and contribute to poor nutrition. and children in the general population of the same age Median. child and family choice.103 Postoperative infection rates. swallowing. Management of motor problems Medical management of motor disorders has changed substantially in the past 30 years. problems with feeding.103 Gastro-oesophageal reflux. aspiration of saliva or gastric contents greatly increases the risk of chest infections. including epilepsy. Reproduced from Dickinson and colleagues.97 Additionally. Successful management balances the social and clinical models of care. botulinum toxin to the salivary glands. has its limits. difficulties encountered are not restricted to an individual’s motor disorder but also to the variety of comorbidities.98 The first randomised controlled trial in this specialty suggested that environmental adjustments for children with physical impairment were at least as effective (as judged by self-help skills and mobility) as conventional therapeutic interventions that aimed to change the child. health and wellbeing.99 Clinical management Overview Two factors are key in management of individuals with cerebral palsy.107 and noted most often in those with severe cerebral palsy and associated severe learning difficulties.104 However. and validated by a multidisciplinary service with the choices of the child and family at the core of decision making.org/ english After controlling for severity of cerebral palsy. myopia. especially if they have more severe forms of cerebral palsy. intake. Quality of life was assessed with the KIDSCREEN questionnaire. Individuals with cerebral palsy usually have comorbidities.thelancet. delay in gastric emptying. families with a high participation in sports).82. In individuals with unilateral spastic cerebral palsy. done. all children should have an ophthalmological assessment. are the objectives.103. including posture. or resiting of salivary ducts. to introduction of new interventions or modification of others. up to 50% have generalised epilepsy for which seizure control can be difficult to achieve. Second.Seminar Physical wellbeing Psychological wellbeing Moods and emotions Self-perception Autonomy Relationships with parents Social support and peers School environment Financial resources Social acceptance 10 50 Score Children in general population 90 Children with cerebral palsy Figure 3: Self-reported quality of life scores by domain for children aged 8−12 years with cerebral palsy. Problems with saliva control are managed by drugs. and social support. partial epilepsy is common.com Vol 383 April 5. which aim to help a family feel in control.

topiramate. 2014 CNS concentrations. Clinical practice has often been based on reports from case series and expert guidelines. associated pain and discomfort. tetrabenazine. it does not cross the blood–brain barrier easily. pattern of motor disorder. and age. The drug has a limited licence in the UK. patients have a dose-dependent risk of side-effects including sedation. thereby reducing focal spasticity. low-voltage stimulation should lead to better organisation of neuro-modulated messages. hypoventilation. patterning. The procedure is done under electrophysiological guidance and is predominantly used in ambulant individuals with bilateral involvement.112.thelancet. Physical. For example. severity. particularly within the globus pallidus. occupational. and carbidopa-levodopa are antidystonic drugs with anticholinergic or dopamine analogue properties used to reduce dystonia by adjusting neurotransmitter bioavailability to the deep cranial nuclei.124 Botulinum toxin A has a particular benefit in children with pain secondary to muscle spasm at the hip.110 the Viking Speech Scale111. partly because of the paucity of randomised controlled trials but also because of the many confounders to treatment such as the effect of comorbidities. a γ-aminobutyric acid (GABA) B agonist that depresses the release of excitatory neurotransmitters at the spinal level.130 Theoretically.109 the Drooling Impact Scale. Paediatric practice aims to reduce secondary musculoskeletal deformity rather than treat the primary central neurological deficit. and lower limb abilities. Their effects might be temporary.119. or stretching. Ordinal classifications and scales used include the Gross Motor Function Classification System.123. or permanent as in most surgical interventions. recent advances in neonatal neuroprotection target babies at high risk of a perinatal hypoxic-ischaemic event. and antiinflammatory agents under investigation increase the neuroprotective effects of these therapeutic approaches. but international guidelines for its use for upper and lower limb spasticity are widely accepted.125 Neurosurgical interventions In selective dorsal rhizotomy.Seminar management to be set and outcomes of trials to be compared. thereby downregulating the overactive spinal reflex.118 Temporary medical interventions Trihexyphenidyl. insufficient studies have been done to date to determine long-term clinical and functional efficacy. Therefore. Appropriate interventions for cerebral palsy are dictated by the patient’s functional ability.135 Erythropoietin is also being used to reduce inflammation and apoptosis and directly stimulate neurogenesis. however. One integrated educational and therapeutic programme is conductive education. postural balance. upper. An acute event precedes secondary cell death and metabolic responses. a randomised clinical trial of conductive education did not show any greater benefits in gross motor function than were noted with traditional physiotherapy approaches.115 however.132 Therapeutic cerebral hypothermia after delivery133 and high-dose maternal magnesium sulfate before delivery134 are given to highrisk term and preterm neonates to reduce the excitooxidative cascade that mediates hypoxic-ischaemic damage. most physical therapies are based on the principles of neuroplasticity.131 Neuroprotection Neuroprotective treatments focus on minimising the brain damage itself. which in turn are followed by ongoing inflammation and epigenetic changes that lead to further damage in the next few months. and melatonin.113 Validated scales also exist for pain.136 Stem cell therapy also aims to reduce these acute and delayed inflammatory responses and stimulate 1245 . Several anticonvulsant. The evidence for most of these interventions is weak. sodium cromoglicate.121 The most commonly used muscle relaxant is baclofen.120 Muscle relaxants work at the spinal and muscle levels to reduce muscle activation by the spinal reflex arc and spasticity occurring because of lack of descending inhibition.127–129 For patients whose motor disorder is purely dyskinetic. the UK’s National Institute for Health and Care Excellence (NICE) panel provided guidelines on spasticity management in children117 and a review of the use of selective dorsal rhizotomy. including phenobarbital. To obtain useful www.com Vol 383 April 5. An adaptive approach is needed to facilitate all developmental domains and reduce the effect of medical problems. Recently. and increased frequency of seizures. some dorsal spinal nerve rootlets are resected.116 Motor interventions aim to change the overactive elements of the upper motor neurone syndrome by reducing the effect of increased muscle tone or improving the fluidity of motor control. but whether this reduction led to improved long-term functional goals was contentious. muscle strengthening. and specific oromotor. patients increasingly have baclofen administered by an intrathecal route with an implantable pump. as with oral medication. Because baclofen is very lipophilic. Comparative analysis between different treatment modalities showed little variation in outcomes. in which quadripolar electrodes are implanted into the basal ganglia. anti-excitatory.122 Botulinum toxin A injections work by blocking the release of acetylcholine at the neuromuscular junction. and two classification systems for communication. researchers are assessing the value of deep brain stimulation.114 they also work in combination with medical management. Different centres use slightly different approaches but they share core principles. and speech and language therapy approaches are essential. allopurinol. A meta-analysis126 of a series of controlled trials confirmed reduction in spasticity. health-related quality of life. To reduce initial injury. inhaled xenon. Evidence of benefit is strongest in the most severely disabled individuals with gross motor function classification system levels IV and V.108 the Manual Ability Classification System.

Van Naarden Braun K. Eur J Epidemiol 2010. Kiely J. eds. 4 Colver AF. Pediatrics 2008. 1967 to 1985. 5 Surveillance of Cerebral Palsy in Europe. early soft and bony tissue surgery has ensured very low rates of subsequent dislocation. Dev Med Child Neurol 2013. Acta Paediatr 2001. Alberman E. Dev Med Child Neurol 2000. Mink JW.137. proportionately more cerebral palsy in children is of postneonatal origin than in developed countries. 111: e89–97. Benedict RE. Trends in perinatal mortality and cerebral palsy in Western Australia. Durkin MS. Arch Dis Child 2003. Management will increasingly focus on promotion of participation and quality of life. A review of the incidence and prevalence. so most treatments are provided by families. contracture formation can lead to reduced mobility. BMJ 1992. AC declares that he has no conflicts of interest. Boulton P.147. and approved the final version. et al. 14 Sellier E. Prevalence of cerebral palsy in 8-year-old children in three areas of the United States in 2002: a multisite collaboration.139 Prevalence of actual dislocation is highest in the non-ambulant population. Dev Med Child Neurol Suppl 2007. such as guidance on how to feed a child with posture and swallowing difficulties146 or multidisciplinary assessment in rural clinics. AC. hip surveillance approaches for children with cerebral palsy involve serial radiographs and examinations. 1862. CF is an unpaid adviser to the European Medicines Agency on treatment of spasticity. At present. and the type and distribution of brain damage such therapy should be directed at is not known. 3 Sanger TD. timing.140. Kirby RS. Surveillance of cerebral palsy in Europe: a collaboration of cerebral palsy surveys and registers. Johnson MA. When hip subluxation is reported. The frequency of cerebral palsy: a review of population studies in industrialised nations since 1950. PODP. 3: 293. 121: 547–54. 9 Pharoah PO. 13 Stanley F. Interventions such as instrumented fusion of the spine to the pelvis by insertion of rods can be undertaken with excellent results in terms of deformity correction but at the expense of significant morbidity in this high-risk group.148 Conclusions In the next decade. embryonic. London: Obstetrical Society of London. Conflicts of interest PODP receives payment for legal reports on the probability of survival in cerebral palsy from several solicitors pursuing litigation in cases of cerebral palsy in the past 3 years. Trends in prevalence of cerebral palsy in children born with a birthweight of 2500 g or over in Europe from 1980 to 1998. Birthweight. 42: 816–24. Several international clinical trials in progress are assessing safety and efficacy of autologous. Prevalence of early childhood disability in a rural district of Sind. Hagberg G. 1246 Improved understanding of brain plasticity will probably lead to new treatments or at least better application of existing ones. 87: 57–68. 11 Ibrahim SH. Mutch L. with accompanying opportunities for prevention and treatment of infection and trauma. 1984–9.thelancet. King R. Prevalence and origin in the birth year period 1991–94. Leviton A. Pakistan. Carefully considered low-cost interventions can be very successful. Individual and societal attitudes will continue to change to recognise that individuals with cerebral palsy have a right not only to inclusion but also to full participation in society and pursuit of their hopes and aspirations. Sethumadhavan T. 2 Rosenbaum P. Arch Dis Child Fetal Neonatal Ed 1998. and CF participated in the planning of the review. recent results of a 5-year follow-up study showed that substantial improvement in gait was not matched by improvements in motor function. Ann Trop Paediatr 2010. In cerebral palsy. difficult labours and asphyxia neonatorum on the mental and physical condition of the child. 12 Paneth N. there is no evidence for clinical application of such therapies in cerebral palsy. 2014 . 55: 357–63. and route of administration are not established.143 However. Paneth N. Surman G. There is some evidence for the benefits of single-event multilevel orthopaedic surgery guided by three-dimensional gait analysis followed by intensive rehabilitation. 109: 8–14.142. wrote and revised the report. 304: 1658–63. and eventually restrict respiratory function. with an expanding range of new technologies directed both to the individual (such as voice synthesisers and robotic assistance) and to the environment (such as intelligent household appliances). 79: F21–25. 10 Gladstone M. Classification and definition of disorders causing hypertonia in childhood. References 1 Little W. Epidemiology of cerebral palsy in England and Scotland. Changing panorama of cerebral palsy in Sweden. Bhutta ZA. Delgado MR. types and aetiology of childhood cerebral palsy in resource-poor settings. Clin Dev Med 1984. Hallett M. 25: 635–42.143 In an ambulant individual. A report: the definition and classification of cerebral palsy April 2006.144 Surgery to lengthen or move contracted muscle-tendon complexes can improve biomechanics and provide stability of the supporting base. 90: 271–77. Contributors PODP is the guarantor of the article and the corresponding author. Gaebler-Spira D. the brain lesions described by the umbrella term cerebral palsy might be classified by their causal factors coupled with a full description of impairments to body structure and functions they produce. Transactions of the Obstetric Society of London. 87: 46–56. In Sweden and Australia. Beckung E. In: Phillips J. or induced pluripotential stem cells. gestational age and the cerebral palsies. Clin Dev Med 1984. Himmelmann K. Doernberg NS. Watson L. dose.Seminar neurogenesis.com Vol 383 April 5.145 Access to clinical care is restricted.138 Orthopaedic interventions The hip joints of individuals with cerebral palsy are at particular risk of displacement. Children with severe cerebral palsy are more likely to die young because of malnutrition and infection.141 Monitoring for scoliosis is essential because the disorder can develop rapidly from a young age in children with severe bilateral spasticity. and the Task Force on Childhood Motor Disorders. especially in relation to deformities. VIII. Management in developing countries Few studies have assessed adults with cerebral palsy in developing countries. 8 Hagberg B. Cooke T. Uvebrant P. 88: 286–90. et al. 7 Stanley FJ. On the influence of abnormal parturition. www. 6 Yeargin-Allsopp M. 30: 181–96. The term diplegia should be abandoned. choice of cell type. In developing countries. Pediatrics 2003.

Grove J. Survival of individuals with cerebral palsy born in Victoria. Neurological damage to the fetus resulting from severe iodine deficiency during pregnancy. Schendel DE. Horber V. UK: National Perinatal Epidemiology Unit. 2: 1038–40. McIntyre S. Endemic cretinism of recent onset in New Guinea. Uldall P. Blair E.thelancet. McAdams AJ. Dev Med Child Neurol 2010. and the Practice Committee of the Child Neurology Society. Pharoah PO. 74: 523–28. McIntyre S. UK: Department of Health. Hum Reprod Update 2009. Cerebral palsy in the surviving twin associated with infant death of the co-twin. Towards the eradication of endemic goitre. Johnson A. Pharoah POD. Pediatrics 1993. London. Dev Med Child Neurol 2001. Dev Med Child Neurol 1997. Weeks BP. New York. Social integration of adults with cerebral palsy. WHO. Hetzel BS. New York. Australia. Obstet Gynecol 2010. J Pediatr 2001. 8: 543–50. www. Australia: Cerebral Palsy Research Institute. Dev Med Child Neurol 2007. Biol Neonate 1999. Monnet E. Twin Res Hum Genet 2005. Hutton JL. Hum Reprod Update 1998. Oxford register of early childhood impairments. Epidemiology of cerebral palsy. Dev Med Child Neurol 2013. National Perinatal Epidemiology Unit. Arch Dis Child Fet Neonatal Ed 2001. Pauchard JY. 48: 643–49. Shatrov JG. Pediatrics 1981. MacLennan A. Semin Fetal Neonatal Med 2006. Dev Med Child Neurol 2008. for the Surveillance of Cerebral Palsy in Europe (SCPE) collaboration of European Cerebral Palsy Registers. 118: 475–82. 75: F174–77. 2002. Pharoah PO. Twins. O’Callaghan ME. 138: 804–10. Blair E. Lancet Neurol 2012. Blasco PA. Jones KL. Pharoah PO. 3: 184–93. Pharoah PO. et al. Geneva. 1995. Fisk N. and the Quality Standards Subcommittee of the American Academy of Neurology. Garne E. Twinning and cerebral palsy: experience in four northern California counties. 52: 345–51. 70: 642–46. Watson L. Friedman AH. Hvidtjørn D. 43: 508–15. Pediatr Res 2011. Grether JK. Croen LA. Congenital anomalies in children with cerebral palsy: a population-based record linkage study. Rankin J. Torrioli M. et al. eds. Dulay AT. Wu YW. Candidate genes and risk for CP: a population-based study. Dev Med Child Neurol 2006. Cooke RW. Strauss D. Nies B. 54: 353–60. TX. birth years 1993–2006. Lancet 2007. Platt MJ. Oxford. between 1970 and 2004. Cans C. Causal hypothesis for some congenital anomalies. 319: 1054–59. Some risk factors for cerebral palsy in very premature infants: importance of premature rupture of membranes and monochorionic twin placentation. Stanley FJ. International classification of functioning. Michael J. Genetic insights into the causes and classification of cerebral palsies. Jarvis S. Quinlivan JA. Dunn J. et al. Alberman E. Hvidtjørn D. J Ultrasound Med 2007. 62: 1106–11. cerebral palsy and congenital anomalies. Michelsen SI. 31: 537–44. United Nations. The vanishing twin: a review. Birch SC. Viteri F. Cerebral palsy and multiple births. Moore CM. 11: 117–25. Watson L. 66: 325–29. 129: e414–23. Reddihough DS. 81: 390–94. 25: 2115–23. Burguet A. NSW. Krägeloh-Mann I. Maclennan AH. cohort study. Stanley F. 2012. Healthcare for all: report of the independent inquiry into access to healthcare for people with learning disabilities London. 92: F489–93. 1989. Schendel D. Obstet Gynecol 1991. 41: 580–85. Evans PM. 91: 254–58. Shavelle R. Florida: University of Miami Press. Sutherland J. disability and health. Vascular etiology of disruptive structural defects in monozygotic twins. Torres AR. UK: Mac Keith Press. Blair E. Pharoah PO. Russman BS. Pharoah PO. Prevalence of congenital heart defects in monochorionic/diamniotic twin gestations: a systematic literature review. cretinism and iodine deficiency. 1st edn. Stanley FJ. Arch Dis Child 2006. Brain Dev 2009. Roebroeck ME. Pediatrics 2012. Daza C. Grove J. births 1983 through 1985. Badawi N. Curry CJ. Lancet 2003. Brooks J. Life expectancy in cerebral palsy: an update. USA: Pan American Health Organization. Causes of excess mortality in cerebral palsy. Congenital abnormalities among children with cerebral palsy: More evidence for prenatal antecedents. Grether JK. Ment Retard Dev Disabil Res Rev 1997. Lancet 1971. 2014 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 Croen LA. Cooke T. Kent RM. and the Australian Collaborative Cerebral Palsy Research Group. BMJ 1999. Prevalence and pathogenesis of congenital anomalies in cerebral palsy. Goldsmith S. Intrauterine disseminated intravascular coagulation: a syndrome of multiple pregnancy with a dead twin fetus. Lam LT. Dev Med Child Neurol 2012. 50: 487–93. Pharoah PO. 75: 177–86. et al. 2013. et al. 369: 43–50. Hutton JL. 1: 308–10. Keogh J. Cummins SK. Cans C. Dev Med Child Neurol 2009. Madsen M. Monozygotic twinning. Hoyme HE. Cans C. Landy HJ. Jahnsen R. Arch Dis Child Fetal Neonatal Ed 1996. Nelson KB. A hypothesis for the aetiology of spastic cerebral palsy—the vanishing twin. Lancet 1974. Hum Reprod 2010. Vanderwerf A. 62: 851–63. Fetal and maternal candidate single nucleotide polymorphism associations with cerebral palsy: a case-control study.com Vol 383 April 5. 84: F111–16. Carlin JB. Pretell E. Badawi N. Ledbetter DH. Chamberlain MA. Convention on the rights of the child. Cause of death in cerebral palsy: a descriptive study. Moreno-De-Luca A. Austin. Freud S. Cerebral palsy update. et al. 2001. Nelson KB. Nelson KB. J Pediatr 1969. Arch Dis Child Fetal Neonatal Ed 2007. Certified cause of death in children and young adults with cerebral palsy. Dundar Y. Life expectancy in severe cerebral palsy. NY. Chorioamnionitis and cerebral palsy: a meta-analysis. 39: 292–96. Acute twin-twin transfusion: a possible mechanism for brain-damaged survivors after intrauterine death of a monochorionic twin. 55: 499–508. Gelfand AA. et al. Pediatrics 2006. 26: 1491–98. Majnemer A. Cable W. 11: 283–92. Blair E. A systematic review of risk factors for cerebral palsy in children born at term in developed countries. 1247 . triplets. 1986. USA: Parthenon Publishing Group. The role of magnetic resonance imaging in elucidating the pathogenesis of cerebral palsy: a systematic review. 4: 177–83. Rosenbloom L. Keith LG. Hansen T. Life expectancy among people with cerebral palsy in Western Australia. McParland P. Buttfield IH. Fusi L. Switzerland: World Health Organisation. 307: 1239–43. Arch Dis Child 1991. Watson L. Shavelle R. Petterson B. Dev Med Child Neurol 1999. Martin CL. 92: 854–58. A template for defining a causal relation between acute intrapartum events and cerebral palsy: international consensus statement. Glinianaia S. Cerebral palsy and intrauterine growth in single births: European collaborative study. Hornabrook RW. Report of the Australian cerebral palsy register. Mendz GL. Higginbottom MC. Cerebral palsy among children born after in vitro fertilization: the role of preterm delivery—a population-based. 15: 639–48. 51: 670–78. USA: United Nations. Landy H. et al. 1968. 116: 387–92.Seminar 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 Maudsley G. Krägeloh-Mann I. Sydney. Carona C. Practice parameter: diagnostic assessment of the child with cerebral palsy: report of the Quality Standards Subcommittee of the American Academy of Neurology and the Practice Committee of the Child Neurology Society. 67: 288–91. 2008. Neurology 2004. BMJ 1993. The vanishing twin. Ashwal S. Wigglesworth J. Strauss D. Pharoah POD. Issues in the classification and epidemiology of cerebral palsy. 1897 [Infantile cerebral paralysis]. Nicolini U. Trends in cerebral palsy among infants of very low birthweight (<1500 g) or born prematurely (<32 weeks) in 16 European centres: a database study. and cerebral palsy in births in Western Australia in the 1980s. Multiplicity and early gestational age contribute to an increased risk of cerebral palsy from assisted conception: a population-based cohort study. Copel JA. Pharoah PO. Adult outcomes and lifespan issues for people with childhood-onset physical disability. Arch Dis Child 1999. Taitz D. Bahtiyar MO. Reid SM. Infantile cerebralähmung. Measures for children with developmental disabilities: an ICF-CY approach. Gibson CS. NY. 78: 517–20. 49: 144–51.

Jarvis SN. Dev Med Child Neurol 2009. Luciano L. Dev Med Child Neurol 2009. randomized controlled trial comparing child. Disabil Rehabil 2008. 53: 1013–18. The Centre for Cerebral Palsy and Cerebral Palsy League of Queensland. Majnemer A. Shevell M. 99: 446–51. Shevell M. Gudmundsson HS. Kirk S. Virella D. 186. Wood E. Johnson HM. Nimigon J. Development of The Viking Speech Scale to classify the speech of children with cerebral palsy. Indredavik MS. Li M. Disabil Rehabil 2013. Cott CA. Child Care Health Dev 2004. Lancet 2007. Does gastrostomy tube feeding increase the risk of respiratory morbidity? Arch Dis Child 2006. Michelsen SI. Dickinson HO.au/docs/documents/FCCS%20and%20 Prompt%20Questions.Seminar 66 67 68 69 70 71 72 73 74 75 76 77 78 79 80 81 82 83 84 85 86 87 88 89 90 1248 Michelsen SI. McEnery G. Pain 2002. Reddihough DS. Law MC. The needs of physically disabled young people during transition to adult services. Rosenbaum PL. Dev Med Child Neurol 2012. Self-reported health status and quality of life in youth with cerebral palsy and typically developing youth. BMJ 1998. Dickinson HO. Carlin J. Dev Med Child Neurol 2011. Shields N. Development and reliability of a system to classify gross motor function in children with cerebral palsy. Rosenbaum P. Paneth N. Predictors of the leisure and recreation participation of children with physical disabilities: a structural equation modeling analysis. von Baeyer CL. Effectiveness of stretch for the treatment and prevention of contractures in people with neurological conditions: a systematic review. Woolfson L. 51 (suppl 4): 16–23. Acta Paediatr 2010. 52: 1056–61. 53: 704–10. 91: 478–82. Hanna S. Eliasson AC. Nieuwstraten W. Eur J Paediatr Neurol 2009. Opheim A. The Manual Ability Classification System (MACS) for children with cerebral palsy: scale development and evidence of validity and reliability. eds. Management of drooling in children. 39: 214–23. Dev Med Child Neurol 2011. Oliver M. Colver A. 53 (suppl 4): 68–70. et al. 51: 105–10. Dev Med Child Neurol 2008. Arch Phys Med Rehabil 2005. Hammal D. Nieuwenhuijsen C. Transitions in the lives of young people with complex healthcare needs. Imms C. Br J Health Psychol 2004. University of Edinburgh. et al. Walter S. pain. The Drooling Impact Scale: a measure of the impact of drooling in children with developmental disabilities. 90: 1891–97. Clinics in developmental medicine no. Self-reported quality of life of 8–12-year-old children with cerebral palsy: a cross-sectional European study. Carona C. 35: 1276–83. Madsen M. Stanghelle JK. Arch Dis Child Pract Ed 2011. Dev Med Child Neurol 2010. Vargus-Adams J. Roebroeck ME. 14: 137–46. 124 (suppl): S1433–35.tccp. 338: b1458. Phys Med Rehabil Clin N Am 2010. Diversity of participation in children with cerebral palsy. Child Health Care 2006. Participation of children with cerebral palsy is influenced by where they live. Morrice J. Uldall P. Dev Med Child Neurol 2009. Watson N. Res Dev Disabil 2013. Participation and enjoyment of leisure activities in school-aged children with cerebral palsy. Family well-being and disabled children: a psychosocial model of disability-related child behaviour problems. Growth and nutritional disorders in children with cerebral palsy. Mjøen T. Behavioural and emotional symptoms of preschool children with cerebral palsy: a population-based study. 30: 317–23. Hadjichristodoulou C.pdf (accessed Oct 11. Arnaud C. Colver AF. Strax TE. Dickinson HO. Cameron K. Gibson L. 91 92 93 94 95 96 97 98 99 100 101 102 103 104 105 106 107 108 109 110 111 112 113 Shikako-Thomas K. Dev Med Child Neurol 2011. Theories in health care and research: theories of disability in health practice and research. Lach L. Ravens-Sieberer U. Psychological problems in children with cerebral palsy: a cross-sectional European study. Kumari S. Self-concept of children with cerebral palsy compared with that of children without impairment. Functional Communication Classification System http://www. Logsdon RG.com. Cerebral palsy and aging. Edinburgh. Visual impairment in children due to damage to the brain. Chamberlain MA. Reid SM. Nutrition and immunity: an overview. Parkinson KN. Switzer L. Krumlinde-Sundholm L. Skjeldal OH. 96: 25–30. Arch Dis Child 2013. Darrah J. Dickinson HO. 99: 281–88. fatigue. Eiriksdottir A. Van Den Berg-Emons RJ. Dev Med Child Neurol 1997. et al. 50: 751–58. Dodd KJ. et al. Roebroeck ME. 317: 1446–49. 98: 434–40. J Nutr 1994. Grant H. Hidecker MJ. Gough M. BMJ 2009. Parkinson KN. Dev Med Child Neurol 2011. Dunn AM. 13: 165–77. Bax M. Majnemer A. Pain in children with cerebral palsy: common triggers and expressive behaviors. 35: 209–34. Children with cerebral palsy participate: a review of the literature. Rosenbaum P. Palisano R. Dutton G. Law M. Youroukos S. Galuppi B. et al. UK: Department of Nursing Studies. Diseth TH. 52: e23–28. Sullivan P. Agarwal P. Continuous postural management and the prevention of deformity in children with cerebral palsy: an appraisal. Fauconnier J.com Vol 383 April 5. Imms C. Participation in life situations of 8–12 year old children with cerebral palsy: cross sectional European study. Barnes C. Stevenson R.versus context-focused intervention for young children with cerebral palsy. Ko B. Dev Med Child Neurol 2006. Epilepsy in patients with cerebral palsy. Murdoch A. Phys Ther 2011. Haak P. 39: 659–63. www. Herbert RD. Pain in young people aged 13 to 17 years with cerebral palsy: cross-sectional. 49: 350–54. Parkinson KN. Dev Med Child Neurol 2010. et al. Nieuwenhuijsen C. Kartin D. Einarsdottir K. Beckung E. Parkes J. 9: 1–13. Pennington L. Chronic pain. 53: 621–29. Dev Med Child Neurol 2004. 54: 836–42. Kuperminc M. Donkervoort M. Life as a disabled child: a qualitative study of young people’s experience and perspectives. 91: 11–24. Family and quality of life: key elements in intervention in children with cerebral palsy. Frequency of participation of 8–12-year-old children with cerebral palsy: a multi-centre cross-sectional European study. The paradox of normalization through rehabilitation: growing up and growing older with cerebral palsy. 89: 121–27. Uldall P. 54: 106–16. I just happen to have a disability”. 51: 670–78. and depressive symptoms in adults with spastic bilateral cerebral palsy. Dickinson HO. 30: 1867–84. Dev Dis Res Rev 2008. 46: 292–98. et al. Van Der Slot WM. J Child Psychol Psychiatry 2008. Jahnsen R. Paneth N. Stam HJ. 34: 567–75. et al. 21: 419–27. multicentre European study. Eltumi M. Dev Med Child Neurol 2012. and fatigue in adults with cerebral palsy: a 7-year follow-up study. Sigurdardottir S. Thomas A. Wiley-Blackwell. and the SPARCLE group. et al. Fehlings D. 49: 405–13. Cunningham-Burley S. Cockerill H. Education and employment prospects in cerebral palsy. Katalinic OM. Colver AF. Law M. 47: 511–17. Harvey LA. McLaughlin J. 51: 381–88. Economic and Social Science Research Council. Chandra RK. and the Transition Research Group South West Netherlands. Shakespeare T. Russell D. Qual Life Res 2009. Lenski M. London: Mac Keith Press. Focus on function: a cluster. 18: 825–32. Experienced problems of young adults with cerebral palsy: targets for rehabilitation care. Pollock N. King G. 2014 . Rösblad B. Flachs EM. 369: 2171–78.thelancet. Fairhurst C. 1999. Reilly S. Vik T. Dev Med Child Neurol 2007. Olsson E. Jahnsen R. Dev Med Child Neurol 2009. Jahnsen R. et al. Kent RM. Arch Phys Med Rehabil 2008. White-Koning M. 50: 363–69. 34: 3202–10. Health-related quality of life in childhood cerebral palsy. Arch Phys Med Rehabil 2009. Dev Med Child Neurol 2008. Lyons A. Ramstad K. Adult outcomes and lifespan issues for people with childhood-onset physical disability. Dodd K. Informing evidence-based clinical practice guidelines for children with cerebral palsy at risk of osteoporosis: a systematic review. Child Care Health Dev 2008. 2010. Developing and validating the Communication Function Classification System for individuals with cerebral palsy. et al. 86: 940–45. 48: 549–54. Vernon-Roberts A. Dev Med Child Neurol 1997. Taylor NF. Walking function. Dev Med Child Neurol 2005. Aging and developmental disability. Quality of life from the perspective of adolescents with cerebral palsy: “I just think I’m a normal kid. Bjornson KF. Hidecker MJ. et al. Belza B. Kejs AMT. Hadden KL. Pain in children with cerebral palsy: a cross-sectional multicentre European study. 2013). Moll LR. Quevedo JP. Hadjipanayis A. Loy Y. Characteristics of recurrent musculoskeletal pain in children with cerebral palsy aged 8 to 18 years.

Effectiveness of physiotherapy and conductive education interventions in children with cerebral palsy: a focused review. J Neurosurg Spine 2010. Mäkelä M. Dev Med Child Neurol 2001. 10: 372–82. A review. 143 Robb J. UK: Springer Verlag. 24: 239–43. Graham HK. Effects of deep brain stimulation in dyskinetic cerebral palsy: a meta-analysis. Bilateral pallidal deep brain stimulation for the treatment of patients with dystonia-choreoathetosis cerebral palsy: a prospective pilot study. 136 McPherson RJ. Dev Med Child Neurol 1998. Guideline 145. The updated European Consensus 2009 on the use of Botulinum toxin for children with cerebral palsy. 2012. Piatt JH Jr. 44: 202–06. Selective dorsal rhizotomy versus orthopedic surgery: a multidimensional assessment of outcome efficacy. Surgical management of spinal deformities in cerebral palsy. Huq S. Lancet Neurol 2011. Lagrange C. et al. Smeeton N. Expert Opin Pharmacother 2010. 24: 336–43. Use of trihexyphenidyl in children with cerebral palsy. 2010: 307–25. and the French SPIDY-2 Study Group. 87: 478–501. Vanderhaeghen P. Moore A. 118 NICE. 148 McConachie H. UK: National Institute for Health and Clinical Excellence. 22: 139–45. Hellmich M. Interventional procedure overview of selective dorsal rhizotomy for spasticity in cerebral palsy. Graham HK. the not as good. 116 Reddihough DS. Erythropoietin for infants with hypoxic-ischemic encephalopathy. Cochrane Database Syst Rev 2009. 53: 13–17. Long-term outcome and adverse effects of selective dorsal rhizotomy in children with cerebral palsy: a systematic review. 40: 749–53. Children’s orthopaedics and fractures. Eur J Paediatr Neurol 2010. Clin Orthop Relat Res 2010. 24: 1200–04. Desloovere K. J Pediatr 2000. Magnesium sulphate for women at risk of preterm birth for neuroprotection of the fetus. 134 Doyle LW.com Vol 383 April 5. Selber P. Middleton P. Feeding difficulties in children with cerebral palsy: low-cost caregiver training in Dhaka. Begum SA. and the possible. London. 119 Cloud LJ. Amini A. Malmivaara A. Ann Neurol 2012. Dev Med Child Neurol 1998. Assessment: Botulinum neurotoxin for the treatment of spasticity (an evidence-based review): report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Vles JS. 137 Gaspard N. Kerr Graham H. Aiona MD. 28: 647–54. Brunner R. 2009. 115 Anttila H. 121 Delgardo M. Consensus on the appropriate use of intrathecal baclofen (ITB) therapy in paediatric spasticity. Love S. 122 Dan B. 142 Sponseller PD. Lancet Neurol 2009. Childs Nerv Syst 2008. 37: 161–67. Management of cerebral palsy. Rehabilitation for children with cerebral palsy in rural Cambodia: parental perceptions of family-centred practices. Hirtz D. Ferdous S. Mov Disord 2013. Newton PO. Gressens P. 40: 763–70. 144 Thomason P. Report of the Quality Standards Sub-Committee of the American Academy of Neurology and Practice Committee of the Child Neurology Society. 1: CD004661. et al. Manchester. 85: 457–65. Dev Med Child Neurol 2011. McConachie H. et al. Marret S. Curr Opin Pediatr 2010. 125 Lundy CT. Thomason P. Pediatr Neurol 2011. et al. 140 Wynter M. Juul SE. Becher JG. Zaman S. Hesketh T. 468: 711–16. Single event multilevel surgery in children with bilateral spastic diplegia: a 5 year prospective study. 102: 385–89. Munir S. Doherty GM. Abel MF. Neurology 2010. 139 Scrutton D. Suoranta J. and the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Comparison between botulinum toxin type A injections and selective posterior rhizotomy in improving gait performance in children with cerebral palsy. 11: 5–15. Yelnik J. 132 Fleiss B. www. A randomized controlled trial of alternative modes of service provision to young children with cerebral palsy in Bangladesh. From stem cells to neural networks: recent advances and perspectives for neurodevelopmental disorders. Delgado MR. 53: 490–98. 14: 45–66. 137: 769–76. Efficacy of programmes based on Conductive Education for young children with cerebral palsy. 2014 131 Koy A. 37: 23–28. Hip dysplasia in bilateral cerebral palsy: incidence and natural history in children aged 18 months to 5 years. UK: National Institute for Health and Clinical Excellence. Am J Phys Med Rehabil 2008. et al. 340: c363. 13: 672–85. 124 Heinen F. Dev Med Child Neurol 2009. Marks M. Arlet V. Dev Med Child Neurol 2011. 7: 586–600. 11: 556–66. Aisen M. Practice parameter: pharmacologic treatment of spasticity in children and adolescents with cerebral palsy (an evidence based review). 127 Kan P. J Child Neurol 2009. Huq S. Pring TR. 1249 . 51: 705–10. Ferdous S. Tertiary mechanisms of brain damage: a new hope for treatment of cerebral palsy? Lancet Neurol 2012. Botulinum toxin type A injections can be an effective treatment for pain in children with hip spasms and cerebral palsy. Neurology 2008. Thomas SS. Brocklehurst P. Arch Phys Med Rehabil 2004. Khan NZ. Gibson N. J Pediatr Rehabil Med 2011. 43: 586–600. Treatment advances in neonatal neuroprotection and neurointensive care. 126 Grunt S. Gooch J. Surgical treatment of spasticity in children: comparison of selective dorsal rhizotomy and intrathecal baclofen pump implantation. 8: 709–17. Gunn AJ. 129 Wong A.Seminar 114 Damiano DL. Coleman G. 117 NICE. et al. Pauls KA. 130 Vidailhet M. Baird G. Clegg NJ. Ashwal S. 135 Johnston MV.thelancet. Autti-Rämö I. The consensus statement on hip surveillance for children with cerebral palsy: Australian standards of care. 128 Buckon CE. Neurological outcomes at 18 months of age after moderate hypothermia for perinatal hypoxic ischaemic encephalopathy: synthesis and meta-analysis of trial data. Motta F. 4: 183–95. Catanese T. 133 Edwards AD. 138 Bennet L. Schroeder AS. et al. Gracies JM. Shah SA. 145 Khan NZ. Fatemi A. Wilson MA. Becher JG. London. 147 Morgan F. Vermuelen RJ. Tan S. 141 Jones-Quaidoo SM. Rehabilitative therapies in cerebral palsy: the good. 123 Simpson DM. 146 Adams MS. 120 Carranza-del Rio J. Wirz SL. Fairhurst CB. Eur J Paediatr Neurol 2010. Jinnah HA. 70: 1691–98. Lui T. Pei Y-C. Van den Heuij L. Bangladesh. Tan B-K. Gait Posture 2013. Sussman MD. Crowther CA. Infection rate after spine surgery in cerebral palsy is high and impairs results: multicenter analysis of risk factors and treatment. Munir S. King J. 38: 878–88. Rouse D. Yang S. Kentish M. et al. Northington F. Mortality of urban and rural young children with cerebral palsy in Bangladesh. Treatment strategies for dystonia. Cell therapy for neonatal hypoxia-ischaemia and cerebral palsy. Vermeulen RJ. Spasticity in children and young people with non-progressive brain disorders. Khan NZ. Letko L. J Neurosurg Pediatr 2005. Child Care Health Dev 2011. Child Care Health Dev 2012. BMJ 2010. 14: 19–28. Report IP318-2.