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Cerebral palsy

Cerebral palsy

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Cerebral palsy
L Andrew Koman, Beth Paterson Smith, Jeffrey S Shilt Cerebral palsy, a range of non-progressive syndromes of posture and motor impairment, is a common cause of disability in childhood. The disorder results from various insults to different areas within the developing nervous system, which partly explains the variability of clinical findings. Management options include physiotherapy, occupational and speech therapy, orthotics, device-assisted modalities, pharmacological intervention, and orthopaedic and neurosurgical procedures. Since 1980, modification of spasticity by means of orally administered drugs, intramuscular chemodenervation agents (alcohol, phenol, botulinum toxin A), intrathecally administered drugs (baclofen), and surgery (neurectomy, rhizotomy) has become more frequent. Family-directed use of holistic approaches for their children with cerebral palsy includes the widespread adoption of complementary and alternative therapies; however, the prevalence of their use and the cost of these options are unknown. Traditional medical techniques (physiotherapy, bracing, and orthopaedic musculoskeletal surgery) remain the mainstay of treatment strategies at this time. This seminar addresses only the musculoskeletal issues associated with cerebral palsy and only indirectly discusses the cognitive, medical, and social issues associated with this diagnosis. Cerebral palsy is the term for a range of non-progressive syndromes of posture and motor impairment that results from an insult to the developing central nervous system (CNS). The characteristic signs are spasticity, movement disorders, muscle weakness, ataxia, and rigidity. Cerebral palsy is the most common cause of severe physical disability in childhood.1 The worldwide prevalence and incidence of the disorder are not clearly known. The overall reported prevalence in children aged 3–10 years is 2·4 per 1000 children, with variability in the reported rates in girls and boys.2,3 During the past 20 years, there have been increases in the incidence and prevalence of cerebral palsy that may be related to improved documentation of cases by national registries, advances in neonatal care, or other factors.4 Cerebral palsy has substantial effects on function and health-related quality of life of patients and their carers; an estimate of the cost of care of patients in the USA in 2002 was US$8·2 billion.5 This seminar aims to outline the epidemiology, pathophysiology, diagnosis, and management of the musculoskeletal manifestations of cerebral palsy. The cognitive, general medical, and societal issues and implications associated with the disorder are not addressed. quadriparesis secondary to rhesus incompatibility, once a common cause of cerebral palsy, is now very low.7 Improved care in neonatal intensive-care units and higher survival for very-low-birthweight infants increases the risk of cerebral palsy.8 Factors linked to the development of the disorder include multiple birth, chorioamnionitis, maternal infection, antepartum vaginal bleeding, second stage of labour lasting longer than 4 h, untreated hyperbilirubinaemia, fetal anoxic events, and fetal infection (especially meningitis or ventriculitis).8–11 The natural course of cerebral palsy has changed greatly during the past 50 years. If appropriate health care is available, affected children without significant comorbidities have actuarial survival approaching that of the general population.12 However, mortality is higher and lifespan shorter in children with severe quadriparesis, hydrocephalus, lack of basic functional skills, refractory seizures, and profound mental retardation.12,13 Associated disorders of CNS-mediated functions are associated with cerebral palsy.14 More than 50% of patients with the disorder can walk without arm assistance; 25% cannot walk, and 30% are mentally

Search strategy and selection criteria
The information in this paper is based primarily on peerreviewed medical publications from 1900 to 2003, relevant textbooks, and appropriate monographs. From 1968 to the present, the databases of the National Library of Medicine were reviewed for appropriate articles. The search term “cerebral palsy” in combination with “surgery,” “alcohol”, “phenol”, “botulinum toxin,” “rhizotomy”, “baclofen”, “diagnosis”, “physical therapy”, “scoliosis”, and “healthrelated quality of life” were used for the initial search. Articles published during the past 5 years were the target of the search. Several earlier, commonly referenced, key publications have been cited. Relevant references cited in the original source references were also reviewed. Several review articles and book chapters were included because they provided comprehensive overviews beyond the scope of this Seminar. Only papers published in English were reviewed. The reference list was modified during the peer-review process on the basis of reviewers’ comments.

Epidemiology and demographics
Cerebral palsy results from an injury in the developing CNS, which can occur in utero, during delivery, or during the first 2 years of life.6 The peripheral manifestations depend on the magnitude, extent, and location of the insult that causes the irreversible damage to the brain, brainstem, or spinal cord. The severity ranges from subtle motor impairment to involvement of the whole body. In more developed countries, the prevalence of athetoid
Lancet 2004; 363: 1619–31
Department of Orthopaedic Surgery, Wake Forest University School of Medicine, Winston-Salem, NC, USA (L A Koman MD, B P Smith PhD, J S Shilt MD) Correspondence to: Dr L Andrew Koman, Department of Orthopaedic Surgery, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157–1070, USA (e-mail: lakoman@wfubmc.edu)

THE LANCET • Vol 363 • May 15, 2004 • www.thelancet.com


For personal use. Only reproduce with permission from The Lancet.

at.24 The motor impairments result from various neurological deficits. and metatarsal varus with hallux valgus. the clinical manifestations of the neurological injuries depend on the extent and type of CNS damage.20 Urinary incontinence is common (23·5%). and diminished proprioception (46%).com For personal use. knee flexion. Reproduced with permission from Wake Forest University Orthopaedic Press. inappropriate involuntary muscle activity associated with upper-motor-neuron paralysis or syndrome.16 Learning disabilities and activity limitations are associated with the degree of cerebral involvement17 and adversely affect school performance. monoplegia. deep CNS hypoxia. so fetal insults occurring during this period can produce periventricular leucomalacia with spastic diplegia. producing spasticity. diplegia. and thumb-in-palm. the loss of descending inhibitory input through the reticulospinal tract and other systems increases the excitability of gamma and alpha neurons.23 Spasticity associated with cerebral palsy can lead to musculoskeletal complications such as contractures. chorea. variations in blood supply and unique metabolic requirements in some brain areas increase the sensitivity to hypoxia in the presence of bacterial or viral infection of the fetus.24 The motor skills of most children with cerebral palsy improve as they grow.4. The leg shows hip adduction/flexion. or within 2 years of birth. and produces abnormal muscle control and weakness. sensory impairment of the arms (97%). dystonia. Hemiplegia is most common in babies born at term and is associated with single hemisphere injury in most cases. decreases the number of effective motor units.10. . but the rate of improvement is slower in children with cerebral palsy than in unaffected children.23 Even though the lesion itself does not change. especially in children and adults with quadriparesis and mental retardation.19 Hemiplegic patients experience abnormal stereognosis (97%).32 which has been defined as a velocity-dependent resistance of muscle to stretch33 or as excessive. some areas of the brain are more susceptible to damage than others. the location of the irreversible insult. which in turn affects motor control. Injury to extrapyramidal systems results in movement disorders such as athetosis. ataxic.29. Figure 1: Typical posture of a child with left hemiparesis The arm assumes a position of internal rotation of the shoulder.21 Pathophysiology Cerebral palsy results from a permanent static lesion of the cerebral motor cortex that occurs before. or rigidity.23 Primary or secondary abnormalities within the spinal cord can increase spasticity. impairment of visual perception (20–40%). Fetal production of cytokines can damage neurons.15 Neurological problems are common and include seizures (35%). and the ability of the CNS to adapt or reorganise after the insult. and peripheral nociception (pain) can also exacerbate it.31 “Selective vulnerability” of the periventricular white matter occurs between 26 weeks and 34 weeks of gestation.25 Similarly.25–31 A specific hypoxic event associated with immediate and irreversible cell death explains the aetiology of cerebral palsy in less than 50% of cases.16 hydrocephalus (9%). Classifications of cerebral palsy are based on: deformity or abnormality (spastic. mixed). For example. autonomic dysfunction. the unique metabolic demands of the basal ganglia in the fetus at 38–40 weeks create “selective” vulnerability that can result in dystonia or movement disorders.35 anatomical distribution of the deformity or abnormality (hemiplegia. preoligodendrocytes. hindfoot valgus. Diplegia is associated with periventricular leucomalacia.SEMINAR impaired. forearm pronation. 1620 THE LANCET • Vol 363 • May 15. whereas movement disorders occur after hyperbilirubinaemia and basal-ganglia injury.11. ankle equines. Ultimately.11 Furthermore. and transient or irreversible ischaemia resulting in cell necrosis secondary to free-radical formation or hypoxia-related metabolic cellular death. diminished two-point discrimination (90%). elbow flexion.34 Quadriplegia is associated with diffuse CNS insults.23 CNS pathology associated with cerebral palsy includes: CNS haemorrhage.28 Injury to upper motor neurons decreases cortical input to the reticulospinal and corticospinal tracts.23 The elimination of spasticity allows many patients with cerebral palsy to use what selective motor control they possess more effectively and functionally. fetal production of cytokines. wrist flexion. and vascular endothelial cells and could contribute to intraventricular haemorrhage. mechanical spinal-cord or brainstem damage. the clinical manifestations of the lesion change as the child grows and develops.10.22. and subluxation.18 and learning disabilities.17. dyskinetic.25–28 or maternal infection or chorioamnionitis. Simultaneously.thelancet. Only reproduce with permission from The Lancet. pain.26. 2004 • www. cerebral cortex hypoxia.

47–49 Observational gait analysis is done with the physician rating scale50–52 or its modified version (the observational gait scale). hip adduction. and joint subluxation or dislocation. or forefoot (metatarsus adductus) deformity. athetosis. hip flexion. flat foot (hindfoot valgus).14 According to this classification system. and Australia. and lordosis. however. elbow flexion.9 from the International Classification of Diseases ninth revision (ICD9). hindfoot valgus. and bunion. Health-related quality of life Measurement of health-related quality of life involves obtaining the patient’s view of his or her health status. kyphosis. these modalities might be valuable for diagnosis and prognosis in the future. Intoeing can result from femoral anteversion. functional MRI and transcranial magnetic stimulation are used only for research purposes in children with cerebral palsy. and quadriplegia (involvement of all four limbs). spinal alignment. Spinal deformities include scoliosis. internal tibial torsion.thelancet.com 1621 For personal use. scissoring (hip adduction). and hemiplegia. several functional instruments and health-related quality-of-life measures have been developed or validated for assessment of patients with cerebral palsy.57. ankle equinus). carers can serve as proxies to provide such information about the child.42 and the functional independence measure in children43 (panel). Currently. and toe flexion are the most common postures (figure 1).SEMINAR quadriplegia). Patterns of spasticity with resultant muscle imbalance across the joints over time can produce shortening of myotendinous units. Some practitioners use this term to suggest asymmetrical involvement or a clearly dominant side. hypotonia. level IV. intoeing or out-toeing. the gross motor performance measure and the paediatric evaluation of disability index are deemed to be two of the best standard measures because they are complementary and test different features of function.4 The Central West Health Planning Information Network (Ontario.53 For children with cerebral palsy. Cranial ultrasonography. impairment. hemiplegia (involvement of the ipsilateral arm and leg). motor power. diplegia 17%.40 With a sample of 408 children. Health-related quality of life includes measures of physical functioning. and ancillary investigations. Similarly. muscle tone (spasticity). 2004 • www. physical examination. Assessment tools and instruments During the past few years. Only reproduce with permission from The Lancet. Diagnosis Diagnosis of cerebral palsy requires a complete history.41 Function Functional capabilities can be assessed by use of global or function-specific instruments. and thumb-in-palm. Most cases of cerebral palsy included in large databases and national reporting registries are identified by the non-specific code 343. Global function instruments include the paediatric evaluation of disability index.61 For young children with cerebral palsy or those with severe involvement. 210 (23%) hemiplegia. symptoms. or disease specific. ankle equinus. sensibility. and hemiplegia 21%. Movement disorders can coexist with the clinical patterns of involvement. 82 (20·1%). is difficult to assess because specific diagnoses are not available. gait (if applicable). forearm pronation.58 The Burke-Fahn-Marsden scale of dystonia59 and the Barry-Albright dystonia scale60 are used to rate the severity of movement disorders. concentrating on symptoms and dysfunction associated with the specific disorder. out-toeing can be secondary to femoral or tibial torsional deformity. level II. joint contracture. knee flexion. 112 (27·5%). described for patients in Sweden. psychological issues. The most common postures observed in the arm are shoulder internal rotation. or extrapyramidal). and there can be spasticity. type and extent of movement disorders.61 Instruments are generic. dystonia (eg. They reported that 45·7% of the patients were classified with the non-specific ICD9 code. jump gait (hip flexion. Movement disorders—dystonia. cortical.0–343. A study in France identified the distribution of clinical patterns as quadriplegia 40%. In the leg. knee flexion. bony deformity. the distribution of the most common clinical patterns. However. USA. the Canchild Centre for Childhood Disability in Ontario reported the numbers and proportions of patients based on the five levels in the gross motor functional classification system: level I. level I indicates few limitations and level V severe impairments. chorea—are common in cerebral palsy. ankle calcaneus). and 402 (44%) quadriplegia. and presence of limb deformity.54 Spasticity and movement disorders Spasticity can be quantified or objectively analysed by the Ashworth spasticity scale. quadriplegia. crouched gait (hip flexion. and other specialised tests are used to assess the extent of the CNS insult. brainstem.56 and the Tardieu scale. . these features are not a prerequisite for its use. MRI. Dynamic deformities and movement disorders can be accentuated during ambulation or other activities. examining all parts of health.64 and the Peds QL 4.65 Classifications Clinical patterns of involvement described in cerebral palsy include: diplegia (significant leg involvement with little effect on the arms). windblown pelvis (fixed adduction contracture in one hip associated with contralateral abduction contracture). The history should include a detailed account of gestation and perinatal events and documentation of the attainment of developmental milestones.62 Three generic instruments suitable for patients with cerebral palsy are the child health questionnaire. knee flexion. 47 (11·5%). pyramidal. wrist flexion. and others are associated primarily with joint subluxation or dislocation or bony abnormalities.36 or location of CNS injury (periventricular.22 Chronological information about the prevalence and time trends of cerebral palsy has been most thoroughly THE LANCET • Vol 363 • May 15. active and passive range of motion of joints. athetosis). In our assessment of 906 children in central and western North Carolina. CT. and disability. 294 (33%) had diplegia. the UK. level III.37–39 However. The term double hemiplegia implies bilateral involvement characterised by greater involvement of the arms than the legs. 86 (21·1%).63 the paediatric musculoskeletal functional health questionnaire. Pathological gait and static abnormalities include: toe walking (ankle equinus). There are three instruments for assessment of arm function44–46 and three for assessment of leg performance. Canada) used ICD9 codes 343.9 to classify 475 children. Some deformities are typically related to imbalance of specific muscles. rigidity. rigidity is rare. 81 (19·9%). or a mixture of these disorders. In addition to a general physical inspection. Dynamic deformities and movement disorders are accentuated during ambulation or activity in many cases.0. and level V.55 the modified Ashworth scale. finger flexion. the examination should assess station (pelvic and leg alignment during stance). social functioning. diplegia.

electrical stimulation). or deformity.69 The best response to heelcord lengthening of the Achilles tendon is seen in patients older than 6 years. Furthermore. These treatments are used to maintain or improve joint range of motion. the frequency of fixed contractures. chemomodulation of spasticity.065 Health-related quality of life in cerebral palsy: diseasespecific instruments Caregiver questionnaire66 Utility measures Health Utilities Index. The treatment options that are used change with the age and developmental stage of the child. provide support. and surgery for management of spasticity associated with cerebral palsy in North Carolina. deviceassisted modalities (eg. and derotation osteotomy procedures have in the best outcomes in children of 8 years old.68 For example.32 Non-pharmacological treatment Non-pharmacological approaches include occupational therapy. 2–6-year-old children show the best response to injections of botulinum toxin. seating systems).66 The functional health status of patients with cerebral palsy has been assessed by the Health Utilities Index-Mark 3 instrument.68 The use of a combination of physiotherapy and orthotics can increase the beneficial effects associated with intramuscular injections of botulinum toxin.69 Children younger than 3 or 4 years rarely develop fixed deformities.32 For successful management. facilitate or strengthen weak muscles.14 which describes health status and health-related quality of life.70 For children who undergo osseous or soft-tissue procedures before skeletal maturity.67 develop. and the need for surgical intervention increases (figure 2).SEMINAR Functional instruments and health-related quality-of-life measures Global function Paediatric evaluation of disability inventory42 Functional independence measure for children43 Arm functional assessment tests/scales Assessment of quality of movement for unilateral upper-limb function (Melbourne)44 Quality of upper extremity skills45 House classification46 Leg functional assessment instruments Gross motor performance measure47 Gross motor functional measure48 Gross motor functional classification system49 Physician rating scale (lower extremity rating scale)50–53 Spasticity assessment instruments Ashworth scale55 Modified Ashworth scale56 Tardieu scale57. and some reports support the use of these injections. orthotics. neuromuscular blocking agents. torsional deformities. the least invasive and most cost-effective treatment should be chosen and the effect of the intervention monitored by use of outcome instruments. or both might be necessary during rapid periods of growth to maintain the benefits of the surgical procedure. dislocation. or any combination of these methods. and those with severe involvement need more extensive interventions.58 Burke-Rahn-Marsden scale of dystonia59 Barry-Albright dystonia scale60 Health-related quality of life in cerebral palsy: generic instruments Child health questionnaire63 Paediatric musculoskeletal-functional health questionnaire64 Peds QL 4. Spasticity management involves the use of a continuum of modalities throughout childhood.thelancet. Skeletally mature children and adults can benefit from chemodenervation (alcohol/phenol) or neuromuscular blockade (botulinum toxin) to manage painful spasticity or to achieve specific functional or positional needs. For example. 2004 • www.32 Most patients with mild involvement receive fewer types of treatments. the consensus is that spasticity associated with cerebral palsy should be treated before children reach the age of 5 or 6 years.com For personal use. and speech therapy. oral pharmacological intervention. casting. In addition. patients’ daily activities can be facilitated by their use of adaptive devices (eg. and surgery. and orthotics in children of this age to modify the natural course of cerebral palsy. improve muscle strength. Treatment of musculoskeletal abnormalities must address one or more of spasticity.69 Treatments should be goal-oriented and produce positive outcomes. muscle stiffness. or bony deformities. As patients grow older. dynamic and static joint deformity. oral pharmacological agents. muscle contracture. physiotherapy. and bony deformity increases. physiotherapy. joint subluxation. the use of intramuscular injections of botulinum toxin to manage focal spasticity might mean that lower doses of orally administered drugs to reduce spasticity are effective. However. Only reproduce with permission from The Lancet. the caregiver questionnaire is the only diseasespecific instrument validated for use in patients with cerebral palsy. inhibit or weaken spastic agonist muscles. therefore. and abnormal motor control. chemodenervation. Mark 314. The severity and distribution of spasticity is crucial to identification of appropriate management options. device-assisted modalities. and improve or normalise motor development. many respond to physiotherapy. Available treatment options include observation. and orthotics.32 100 90 80 70 60 50 40 30 20 10 0 0 Non-surgical Chemodenervation Surgery To date. standers. 1622 THE LANCET • Vol 363 • May 15. so that contractures do not have the chance to Frequency of use (%) 2 4 6 8 10 12 14 16 18 Age of patient (years) Figure 2: Use of non-surgical treatments (physiotherapy and occupational therapy). 1999–2002 Reproduced with permission from Wake Forest University Orthopaedic Press. physiotherapy. joint contractures. the interventions should be adjusted on the basis of efficacy in achieving preintervention goals and the carers’ adherence to the prescribed therapeutic interventions. casting. parenteral medication. .32 most patients are managed with a combination of modalities.67 Management options The spasticity management technique used for children with cerebral palsy is determined primarily by the clinical findings.

Pharmacological options Various orally. placebo-controlled. Braces are used for young cerebral-palsy patients with scoliosis to delay surgical management until the children reach skeletal maturity. to provide joint stability. Therapeutic modalities Various approaches are used to facilitate range of motion. improved muscle strength becomes evident and measurable within 1–2 weeks after the start of treatment. increase stride and step length. orthotics improve ankle kinematics and kinetics. spinal orthotics and chair inserts rarely halt curve progression once the curve has exceeded 40° and are used primarily for positioning. further research is needed to define the long-term effects of this intervention in patients with cerebral palsy. There are several different types including the traditional solid orthosis. pneumothorax. The most common device is the ankle- foot orthosis.75. Functional electrical stimulation combined with dynamic bracing improves arm function. including ear pain.99 Customised wheelchair inserts or orthotics are used for passive correction of scoliosis. placebo-controlled trial of this therapy found that hyperbaric oxygen did not improve the condition of children with cerebral palsy compared with slightly pressurised air. to facilitate therapy.103 No significant difference was found between the groups in results of neuropsychological testing. Improved function during brace wear in patients with spastic arms. the latter is licensed for use THE LANCET • Vol 363 • May 15.71–73 However. myopia.24 However. Exceptions include intrathecal baclofen and botulinum toxin A. The former is labelled for children with cerebral palsy in the USA. and intrathecally administered pharmacological options are available to manage spasticity.95 Various features to decrease tone or spasticity are attributed to orthotic use. However.92 In contrast to therapeutic approaches.85 Constraint-induced therapy treatment models developed for rehabilitation of the arm in adults with stroke are now under investigation for use in patients with cerebral palsy. However. the hinged orthosis. there is little evidence-based information supporting or refuting their value in the management of cerebral palsy. and kyphosis are used. and orthotics. controlled study. splinting. critics argue that the placebo treatment in some trials constituted therapeutic amounts of oxygen and that the hyperbaric treatment is beneficial. however. and/or speech).84. leg orthotics or splinting can provide significant functional advantage by stabilising joints during standing or ambulation as well as by maintaining muscle resting length. Preliminary case studies or trials with small numbers of patients suggest that constraint-induced therapy results in improvements in hand function. placebo-controlled trial in 75 children. many internet sites provide information about this therapy.81 paediatric massage. intramuscularly. However.84. and improve function. In patients without ankle or hindfoot contracture. and variable rigidity to address the specific requirements for each patient. quadriparetic involvement.91. and the posterior leaf spring orthosis. Only reproduce with permission from The Lancet. to prevent or delay contractures.83 and constraint-induced movement. Orthotics are made from various materials and incorporate hinges.SEMINAR Therapeutic intervention Most children with cerebral palsy receive therapy of some type (physiotherapy. .94 Arm orthotics are mainly used to maintain myotendinous length. the only group for which bracing may be effective is a small subset of ambulatory patients with spasticity and significant weakness. lordosis.76 patterning. with the exception of ring splints for swan-neck deformity. Neuromuscular electrical stimulation is classified as therapeutic89 or functional. months of this treatment can be needed for efficacy. most reports suggest no effect of brace wearing on the progression of significant spinal deformities. to maintain range of motion.82 Adelphi Polish Suit Program.86–88 However.101. The use of soft spinal orthoses instead of rigid orthoses increases the likelihood that they will be worn. 100% oxygen at 1·75 atmospheres absolute for 40 sessions was compared with air at 1·30 atmospheres absolute for 40 sessions. casting. no improvement in objectively measured function was documented when therapeutic electrical stimulation was compared with placebo treatment.98 Poor adherence to brace wearing may have a role in the failure of spinal orthotics. hyperbaric oxygen therapy should be considered an experimental intervention until further randomised. splinting is used to maintain muscle length. the stimulus used with functional electrical stimulation produces a visible muscle contraction. and fire and explosions associated with the equipment. Although there have been many publications on these therapies. damage to the ear. occupational.102 However. Physiotherapy and occupational therapy interventions include a wide range of techniques and schools including classic neurodevelopmental therapy techniques.80 Vojta techniques. and lumbar curves.90 Therapeutic electrical stimulation uses daily low exposure of spastic muscles. to maximise activity.24 On the basis of the current peer-reviewed scientific data. or to maintain the effects of chemodenervation or surgery. most of the agents routinely used by patients with cerebral palsy are not labelled for paediatric use.93 and functional electrical stimulation of the anterior compartment of the leg combined with injection of botulinum toxin A in the gastrocnemius resulted in improved ambulation and reduced muscle tone in adults with spastic equinus gait. Serial casting is a non-surgical method to increase musculotendinous length. and to normalise function.74 Strength training has been advocated to promote fitness and increase patients’ participation in various recreational and occupational activities. However. successful medical and surgical interventions generally depend on physiotherapy and occupational therapy for maximum benefit. springs. and orthotics are used to provide stability.78 hippotherapy.thelancet. and Commonwealth nations. western Europe. is rare.77 conductive education. With compliant patients.100 Hyperbaric oxygen Hyperbaric oxygen therapy is used by some patients despite the lack of scientific validation of its efficacy.101 In another double-blind. In a randomised. These include electrical stimulation. but they are less effective in patients with neuromuscular spinal deformity than in patients with idiopathic scoliosis. improve coordination.com 1623 For personal use. and provision of head and neck support. The largest randomised. and some insurance companies will cover its costs. convulsions. parents of children treated with air reported better results than the parents of those treated with hyperbaric oxygen.96 Rigid or soft orthotics designed to maintain or to correct scoliosis. scientific support to validate the use of most orthotics or their effect on the natural course of most deformities in cerebral palsy is lacking.79 aquatics. If functional electrical stimulation is effective. stabilisation of the trunk.73 Muscle strengthening has been associated with improved function in patients with cerebral palsy. double-blind trials are completed. to delay or prevent deformity.97. and to encourage adaptive mechanisms. however. 2004 • www. Hyperbaric oxygen therapy is associated with various risks.

therapists. physician. the area of effective denervation extends just a few millimetres from the injection site. and phenol.SEMINAR in children with cerebral palsy in 44 countries but not the USA. These agents include botulinum toxins.23 The computer software used with the pump can be programmed to deliver different amounts of drug during the day depending on the degree of spasticity reduction that is required for different activities. Neuromuscular blockade/chemodenervation Injectable neuromuscular blocking agents balance muscle power across joints by producing selective denervation of muscles and nerves. comfort. and endurance. Parenterally administered agents used to manage spasticity in children with cerebral palsy include baclofen. In fact. Only reproduce with permission from The Lancet. Side-effects of alcohol and phenol injections include pain on Light chain Synaptic vesicle injection. reproduced with permission from Wake Forest University individual muscles depends on the Orthopaedic Press. intrathecal baclofen has produced variable beneficial effects on arm spasticity105 and. joint imbalance secondary to spasticity. formed Compared with phenol injections. and dural leakage). documented spasticity reduction during a trial shows the patient’s responsiveness to the drug.thelancet. and other care providers is essential during the trial process to ensure that everyone sets realistic goals for the treatment. synaptobrevin. 2004 • www.104 Indications for intrathecal baclofen include: impaired gait and leg movement in patients without significant weakness. However. dislodgement. anecdotally. patient. 114 1624 THE LANCET • Vol 363 • May 15. in each patient an intrathecal trial with either a single bolus or short-term infusion of baclofen should be done. and family to meet each individual patient’s needs. Decreased tone interfering with function during the trial of intrathecal baclofen is not a contraindication to pump implantation. and ease of drug administration. the management of spasticity in children is not one of the labelled indications for use. haematoma.108.110 complex Synaptobrevin Botulinum toxin A can be injected not intramuscularly to produce selective Heavy formed SNAP 25 Synaptic chain and reversible chemodenervation at fusion complex the neuromuscular junction (figure 3). and diazepam are examples of the most frequently prescribed medications. within the neuromuscular junctions and the mechanism of action of botulinum toxins Injections of botulinum toxin A are on the synaptic fusion complex used in the management of focal SNARE proteins (SNAP-25. erosion. F. tizanidine. rupture. Adapted from Arnon et al. injections of botulinum toxin are associated with fewer complications. delivery of the drug can be modulated according to the degree of spasticity and weakness best suited for each individual patient to avoid interference with functioning. however.com For personal use. and pumps must be refilled with drug at a minimum of every 3 months. the pumps are programmed with input from the therapist. generalised spasticity in appropriately selected patients with spasticity and movement disorders. 2001. and seizure medications. The frequency of pump refills is mandated by the fluid capacity of the pump and the limited stability of baclofen in solution. toxin C affects both SNAP-25 and syntaxin. decubitus. and G cleave selective dorsal rhizotomy are used to synaptobrevin. . possible permanent muscle SNARE fibrosis. botulinum toxins. however.110–113 Phenol and alcohol are non-selective proteolytic agents and produce selective denervation when injected into motor nerves or muscles. blockage. intrathecal baclofen and containing vesicle to the cell membrane and release of the neurotransmitter. spastic quadriparesis in non-ambulatory patients that interferes with function. and dysaesthesias lasting for proteins SNARE several weeks. phenol (3–7%). activities of daily living. whereas phenol denervation lasts 4–8 months. Release of acetylcholine produces muscle contraction.68 Botulinum Acetylcholine toxin A has been used clinically in the Muscle cell Synaptic Synaptic does not management of spasticity associated cleft cleft Muscle cell contract with cerebral palsy since 1988. Toxins A and E cleave SNAP-25. Intrathecal infusion of baclofen is effective in reducing tone. is reported to improve speech. painful or function-limiting dystonia. The duration of denervation associated with alcohol injection is 3–6 months. and syntaxin) are necessary for fusion of the acetylcholinespasticity. In addition to decreasing spasticity in the legs. D. toxins B. non-selective protein denaturation. A successful trial supporting implantation of a baclofen pump is defined as a reduction of at least 1 point on the Ashworth spasticity scale. Replacement of pumps is required every 5–7 years. the short half-life of the drug means that it has to be infused continuously for optimum spasticity management. the pump can be adjusted to deliver one dose of drug during sleep and to lower the dose during the day to facilitate function. Because diffusion of both is limited. Alcohol and phenol injections also are used to assess the effect of spasticity reduction in potential candidates for surgery.104 To test whether intrathecal baclofen is suitable. arm and leg spasticity interfering with function. Orally administered medications used to treat spasticity include GABA agonists. and spasticity interfering with carers’ support activities in nonfunctional children. alcohol. Once a pump is implanted. Complications associated with intrathecal baclofen can be caused by the pump placement (seroma. the criteria to identify the best candidates for this therapy have not been defined completely. infection) or the catheter (migration. Indications for alcohol and phenol injections include spasticity.115 The toxin is injected into spastic muscles Figure 3: Schematic representation of the normal mechanism of acetylcholine release to balance muscle forces across joints. For example. Acetylcholine Syntaxin receptor greater reversibility of effects. 2-adrenergic agonists.104 Intrathecal baclofen is an effective treatment for management of severe. wound breakdown.107–109 and alcohol (45–100%). and decreased function.106 The level of catheter placement within the spinal cord can be adjusted to modulate the effects on arm versus leg control of tone. Failure to produce an effective synaptic manage more widespread spasticity. Baclofen.69 fusion complex prevents vesicle attachment and the release of acetylcholine and produces flaccid The amount of toxin injected into paralysis. muscle relaxants. The participation of parents.

double-blind dose-ranging studies have examined the effects of various doses of Botox125 or Dysport118. postoperative or post-treatment pain control.32 Common reported sideeffects include muscle soreness. single-blind trial confirmed these findings. a study of children with cerebral palsy and equinus showed that a combination of injections of botulinum toxin A and functional electrical stimulation did not result in better outcomes than treatment with toxin injections alone.thelancet.128 One trial assessed whether toxin injections were more effective when given before or after casting.32.130 The combination of toxin Figure 4: Schematic representation of the technique of selected dorsal rhizotomy A: after laminectomy. hamstring tightness. although functional changes were negligible.120 Patients receiving toxin showed increased range of motion and decreased tone. the facet joints are excluded. if possible. Although there are no standard guidelines on doses in children.116 The doses of these two commercial preparations are not interchangeable.SEMINAR formulation of the toxin.52.5 and drooling reduction. Only reproduce with permission from The Lancet. infection. Botox is used most commonly in concentrations of 50 U/mL or 100 U/mL. and the duration of its effect is speculative. The rootlets are stimulated so that abnormal rootlet activity can be identified.135 Surgical reduction of spasticity The use of selective dorsal rhizotomy for spasticity management was first reported in cerebral palsy in 1981.136 This operation decreases spasticity by balancing spinalcord-mediated facilitory and inhibitory control (figure 4). Botox is approved and licensed for use in cerebral palsy in 44 countries. Doses of 2–6 U/kg bodyweight per muscle with a maximum total dose of 29 U/kg have been reported. as measured by gait analysis. This procedure involves stimulation and transection of selective posterior rootlets or arbitrary transection of a specific proportion of rootlets.5 Botulinum toxin A has an excellent safety profile with a low frequency of side-effects. UK). as a diagnostic trial. One study investigated the effect on arm range of motion and function.116 Overall.126 on gait measures in patients with cerebral palsy. The current practice is to inject several muscles at each injection session. B: a proportion of rootlets are transected.69.127. The procedure requires a laminectomy at L2–L5. Subsequent selective dorsal rhizotomy THE LANCET • Vol 363 • May 15.124 The final randomised. Two prospective. double-blind. double-blind. rash.118. with smaller patients receiving higher doses than reported in the past. influenza-like symptoms.133 Adverse events seem to be related to the total dose administered rather than the dose calculated on the basis of the patient’s bodyweight.94 However.129 Slightly better outcomes. . and the size and weight of the patient. randomised trials have shown the efficacy of botulinum toxin A as a substitute for serial casting in equinus deformity.134 A contraindication for these injections is the presence of a fixed contracture. injections and use of a hip orthotic improved gait compared with physiotherapy and “best practice” in a randomised prospective trial. 2004 • www.128 The use of functional electrical stimulation combined with botulinum toxin A was superior to functional electrical stimulation alone in one short-term study of patients with stroke.126 Indications for intramuscular botulinum toxin A injections in patients with cerebral palsy include: dynamic deformity interfering with function. easing of the burden on carers. to prevent spinal-column instability and secondary deformity.117 a review of previous publications indicates that the dose that has been used for children with cerebral palsy has increased over time.119 Three randomised. Reproduced with permission from Wake Forest University Orthopaedic Press.120–123 Patients who received toxin injections responded with improved ambulatory status. were observed in patients whose casts were applied after the toxin injections. the size of the muscle. scissoring. excessive weakness. symptomatic focal dystonia. placebo-controlled trials have shown the efficacy and safety of botulinum toxin A in the management of spasticity associated with cerebral palsy. and improved health-related quality of life.52.5 1 U Botox is equivalent to about 3–5 U Dysport. Dysport is not approved for use in the USA. painful spasticity with or without fixed muscle contracture. placebo-controlled study showed that patients with cerebral palsy who underwent hip surgery needed less morphine and codeine to manage their postoperative pain if the hip muscles were injected with botulinum toxin A before surgery. Two formulations of botulinum toxin A are available for intramuscular injection: Botox (Allergan. muscle imbalance producing or contributing to skeletal deformity. producing pain. both Dysport and Botox have a satisfactory safety profile. The recommended dose of Dysport for children is 30 U/kg bodyweight up to a maximum of 1000 U. although it is not approved for management of spasticity associated with cerebral palsy by the Food and Drug Administration in the USA. In these studies. Irvine. the optimum dose is unknown.121. the dura is opened and the dorsal spinal rootlets are exposed. USA) and Dysport (Ipsen Limited. Maidenhead.5 Seven randomised.68 Type B toxin is a different serotype from type A toxin and is commercially available as Myobloc (USA) or Neurobloc (Europe).118. there are no peer-reviewed publications describing its use.131 Other prospective data support the use of botulinum toxin A in the management of crouched gait. the higher doses of the preparations were more effective in improving gait measures than the lower doses. fatigue. or contributing to progressive deformity. Berkshire. since they are ineffective in this case.68 Although type B toxin has been used for spasticity management in cerebral palsy.132.com 1625 For personal use. CA.118–123 Five of the studies assessed the effect of toxin injections on leg spasticity in ambulatory patients with cerebral palsy. and allergic reaction. A second randomised. pain on injection. the number of neuromuscular junctions in the muscle.

100 Progression of curves beyond 50° is frequent.SEMINAR approaches have used two-level laminectomies. No randomised controlled studies have identified optimum surgical combinations or supported the use of one surgical option over another. overlengthened tendons. or stabilise spinal deformity.141 whereas others believe that it causes accelerated hip subluxation. kyphosis and lordosis are not associated with significant comorbidity. less commonly. tenotomy.139 A meta-analysis of three randomised. comorbidities. restore. In 1995.151 A progressive spinal curve deformity between 40° and 50° in a growing child and documented progression of a curve beyond 50° after skeletal maturity are indications for surgery in patients with favourable risk/benefit ratios. many patients require orthotics and long-term physiotherapy to achieve the best outcome.138 Because transient muscle weakness is observed after the procedure. dystonic. with the rate approaching 60–75% in patients with severe involvement and quadriplegia. controversy remains over whether selective dorsal rhizotomy reduces the need for subsequent orthopaedic procedures.142 increases pelvic tilt in ambulatory patients. Other outcomes included muscle strength.146 Therefore. A randomised single-blind trial of 30 patients showed that patients assigned rhizotomy and intensive outpatient physiotherapy for 9 months experienced better outcomes than those assigned intensive physiotherapy alone. Preoperative discussions with the patients’ parents or carers 1626 THE LANCET • Vol 363 • May 15.144 Furthermore. refractory spinal deformity. diminish painful spasticity.148 Anterior and posterior spinal instrumentation and fusion might be necessary for adequate correction of spinal alignment to be achieved and the risk of non-union kept to a minimum. ataxia. Some researchers believe that early use of the procedure reduces the need for orthopaedic procedures. The irreversibility of the procedure dictates caution when this therapeutic modality is chosen. and lordosis) are associated with cerebral palsy. fuse unstable joints by arthrodesis. Renshaw and colleagues100 stated that “rhizotomy is not indicated in the presence of athetosis. Neuromuscular blockade of the concave paraspinal musculature has been attempted with varying success (anecdoctal reports). Delays in surgery that do not compromise function and health-related quality of life are recommended to avoid recurrence of the deformity and the unpredictable results common in younger children related to their growth potential.140 In addition.146 Conversely. No randomised prospective trials comparing surgery with observation have been published. good strength. balance joint forces. The natural course of a specific musculoskeletal deformity should be factored into the surgical decision-making process. Spinal deformity Deformities of the spine (scoliosis. muscle weakness. 2004 • www.147. pure spasticity. osteotomy. difficulty in sitting. heelcord surgery done in children over the age of 6·5 years results in improved function and is associated with little recurrence of the equinus deformity.137.148 The natural course of scoliosis in cerebral palsy differs from that of idiopathic scoliosis and is characterised by curve progression after skeletal maturity. multisegmental spinal fusion. others prefer to operate on children older than 6–8 years. fixed contractures. dystonia. disease severity.139 Therefore. arthrodesis. fractional myotendinous lengthening. Only reproduce with permission from The Lancet. range of motion. with curves beyond 100° a risk factor for complications. adductor tenotomy and iliopsoas recession in a child with 50% subluxation of the femoral head will prevent dislocation and will improve hip stability and coverage in over 80% of children. no fixed contractures.thelancet. cardiopulmonary compromise. and. diplegia.143 and exaggerates lumbar lordosis and speeds progression of scoliosis. no studies have compared two or more surgical procedures for the management of specific deformities. Furthermore. The primary outcome measure was the total score on the gross motor function measure. ostectomy. early and prompt treatment of hip subluxation at an earlier age is appropriate. and improves outcome in selected patients.149. no prospective trials have documented the effects of intrathecal baclofen on spinal biomechanics.151 Bracing of patients with neuromuscular scoliosis is unsuccessful in many cases. and painful arthritis. the observed improvement in motor function could not be explained by the intensive physiotherapy programme. and severe neurological involvement. untreated hip subluxation can progress to hip dislocation. Both an increase in lumbar lordosis and progression of scoliosis have been reported after rhizotomy144 and implantation of an intrathecal baclofen pump. tendon transfer. decreases the period of postoperative immobilisation and the rate of nonunion.148 Postoperative complications of spine surgery are common in patients with excessive curvature. Most of the indications for orthopaedic surgery in patients with cerebral palsy are based on retrospective reviews that include non-concurrent or historical controls. Patients with normal intelligence. nutritional compromise. controlled trials concluded that selective dorsal rhizotomy and physiotherapy provided a small but significant increase in scores on the gross motor function measure compared with physiotherapy alone. The surgical procedures should be individually adjusted according to the patient’s age. transfer motor power. or mixed). and deformity preventing adequate administration of care. Indications for surgery include progressive deformity producing pain or interfering with function. and physiological cost index. and paraspinal muscle-strengthening programmes do not improve outcome. muscle tone. pelvic obliquity. kyphosis. Orthopaedic surgery Long-established orthopaedic surgical procedures are designed to lengthen contracted myotendinous units. rigidity.145 For example. and maintain.70 However. Our own experience suggests a need for careful documentation of existing spinal deformity before pump placement and careful radiographic monitoring of the patient’s spine twice a year after pump implantation. and postural stability have been identified as the best candidates for selective dorsal rhizotomy. and overall well-being.152 However. we have seen extreme hindfoot valgus and midfoot collapse in young children after the procedure. reduce joint subluxation and dislocation to improve joint congruency. . underlying pathology (spastic. Orthopaedic surgical techniques include neurectomy. tendon lengthening. electrical stimulation of the convex paraspinal musculature has not been successful.com For personal use. joint subluxation or dislocation.32 The ideal age and best technique for selective dorsal rhizotomy are unknown. interference with sitting.150 Progression of scoliosis can lead to pain. or severe fixed joint contracture”.148 The use of segmental spinal instrumentation improves correction. or a combination of these procedures. although the exact indications are difficult to define from the existing evidence. Although scoliosis can lead to serious outcomes. correct bony deformity to improve biomechanical alignment. Some surgeons undertake the procedure in children aged 2–4 years.100 The overall frequency of scoliosis in cerebral palsy is 25%.

knee flexion. and abductor pollicis longus.23 Intrathecal baclofen and rhizotomy can decrease arm spasticity and positively affect function. if present: joint stability (capsulodesis170 or arthrodesis158). anterior elbow release in selected patients reduces flexion posture angle without increasing maximum flexion. improve function.16 Furthermore. although contractures of 30–60° might benefit from surgical intervention. THE LANCET • Vol 363 • May 15. or rerouting of the pronator teres. However. to improve joint alignment or congruency. humeral osteotomy. wrist arthrodesis.171 dorsal release of the adductor and first dorsal interosseous from the first and second metacarpals. and volitional control. flexor tendon transfers to the wrist or digit extensors.157 However.158 Reduced sensitivity is common in patients with spastic arms as shown by deficits in stereognosis (97%). and joint reduction with capsulodesis. Leg surgery Surgical procedures for the legs are designed to improve ambulation.162 or plication. The role of surgery is not as prominent for arm deformities as for the legs because of sensory impairments associated with spasticity of the arms and the limited functional gains after surgery. and some sensibility.105. internal rotation of the hip.SEMINAR about the possible effect of pump placement on the progression of spinal deformity are imperative. Concomitant pump implantation and spinal fusion have been done in patients with pre-existing spine deformities.157. arthrodesis.158. Thumb-in-palm deformity is multifactorial. and humeral osteotomy. ankle equinus. to prevent or delay arthritis or progressive deformity. A deformity of less than 30° rarely justifies surgery. metacarpal phalangeal hyperextension or global instability. continuous electromyographic activity of the flexor carpi ulnaris supports the transfer of this muscle to the finger extensors rather than a wrist extensor. The procedure used depends on the patient’s age.164–167 Wrist extension can be improved by: transfer of a wrist flexor to a wrist extensor or finger extensor. joint congruency.169 Figure 5: Thumb-in-palm deformity The deformity is complex and can include: soft-tissue contracture of the thumb–index web. The walking pattern of patients with cerebral palsy is inefficient and abnormal as a result of increased muscle tone in the legs associated with increased pelvic tilt. hip adduction.thelancet. and to improve activities of daily living.157 Electromyography of the forearm muscles can facilitate the selection of the appropriate surgical option. Reproduced with permission from Wake Forest University Orthopaedic Press. 2004 • www. or both. skin contracture (four-flap Z plasty or skin graft158. to improve self-care and self-esteem. two-point discrimination (90%). decrease pain. movement disorders.168. splinting. and planovalgus foot deformity.159 Functional deficits are observed in 80% of limbs in children with hemiplegia and quadriplegia.153. tendon lengthening. or joint incongruity are candidates for soft-tissue procedures. neurectomy.16. to facilitate or decrease orthotic use. extrinsic motor imbalance with overlengthening and/or weakness of the extension pollicis longus. extensor pollicis brevis.162 Surgical procedures for thumb and finger deformities provide predictable beneficial results for children and adults who have spasticity. hip flexion.158. improves function. proximal row carpectomy. In general.162 lengthening or reinforcement of the flexor pollicis longus. The goals of these procedures are: to improve ambulation by improving quality of gait. some voluntary motor control. first dorsal interosseous. finger flexion deformity. tendon transfer.157. and proprioception (46%).96 Surgical options include tenotomy. and contracture of the first web space represent the most common thumb and finger deformities in patients with cerebral palsy (figure 5). or both (release of the origin of the adductor). capsulodesis.157 In general. decrease spasticity. For example. intrinsic motor contracture and spasticity. and surgical management of this deformity must therefore address the following.163 Osseous procedures are rarely indicated to manage elbow flexion. osteotomy. and improves appearance and selfesteem. lengthening.163 Forearm pronation deformity can be decreased by tenotomy. Postoperative care.com 1627 For personal use. is important for optimum surgical outcomes. and improve health-related quality of life. including hand therapy.153–156 Soft-tissue procedures are rarely successful in patients with movement disorders. or shoulder fusion. swan-neck deformity. others may need bony options. Arms Surgical management of the arms in patients with cerebral palsy is designed to correct muscle contracture. sensory reeducation.162 transfer of the adductor insertion to the metacarpal. and pronator flexor slide. patients with movement disorders who lack voluntary motor control and sensibility experience inconsistent postoperative results. to facilitate care. extent of motor involvement.158. to decrease pain by reducing spasticity. Z plasty of the biceps brachii. reduce deformity. Thumb-in-palm deformity. transfer of the extensor carpi ulnaris to the fourth metacarpal. and strengthening programmes. Shoulder fusion is rarely indicated. Patients with elbow flexion contractures of greater than 60° are candidates for surgery if the goals of patient and physician are reasonable. only 10–15% of these patients are candidates for corrective musculoskeletal surgery.158. increases active extension. intrinsic-muscle overactivity. transfer of the latissimus dorsi and teres major tendons to the lateral humerus. arthrodesis can improve outcomes in these patients. Weakening biceps function may exacerbate pronation deformities and must be factored into any surgical decision.158.158 By contrast. contracture of the adductor pollicis. Significant elbow flexion contracture can be decreased by any permutation of the following: brachialis fractional lengthening.162). neurectomy procedures are avoided.162 Deformities of the fingers can be managed by arthrodesis. and contracture and/or weakness of the flexor pollicis longus. Only reproduce with permission from The Lancet. bony architecture. rerouting. joint instability.160 A preliminary report of C8 root division documented reduced muscle tone in wrist and finger flexors.168 or a combination of these options.161 Shoulder internal rotation can be managed by: lengthening of the pectoralis major or subscapularis tendons.157. .156. or reinforcement of the extrinsic thumb extensors and abductors. flexor-pronator slide. release of the elbow capsule.162 Younger patients without arthritis. the extent of sensory loss does not correlate directly with the severity of the motor deficit. or intrinsic/extrinsic rebalancing.157. or facilitate care activities.

Blair E. Beckung E. lengthening of both the aponeurosis of the gastrocnemius and soleus. Rumeau-Rouquette C. Curr Opin Pediatr 1997. Alberman E.175 calcaneal lengthening. 44: 240–47. and reduction of discomfort. The most common combined deformity is hindfoot equinovalgus and midfoot pronation.178. Verrier A.22 Management of hip deformity is dictated by the extent of deformity and the time it has been present. 18: 278–81. Dev Med Child Neurol 2002. metatarsus primus varus. Prevalence and disabilities in 4 to 8 year olds with cerebral palsy. or rarely neurectomy. Prevalence and health impact of developmental disabilities in US children. Cerebral palsy. Rumeau-Rouquette C. In patients under the age of 7 years. 194–95. Curr Opin Neurol 2000. A painful dislocated hip is commonly treated by non-operative management (analgesics. and supination or pronation of the midfoot-forefoot complex. Vandenbussche E. du MC. Pediatrics 1998. Murphy CC. hip dislocation or significant subluxation is managed with varus derotation osteotomy alone or combined with pelvic osteotomy and open reduction capsular plication and adductor release. 40: 369–75. Balkrishnan R. 42: 816–24. Health status of school-aged children with cerebral palsy: information from a population-based sample.172–174 Equinus ankle deformity can be complicated by coexisting deformities including hindfoot varus. Grandjean H. and sensory disabilities on survival in cerebral palsy. Grether JK.183. Cans C. tendon transfer. anti-spasticity drugs) is unsuccessful. Int J Epidemiol 1997. Dabney KW. Morb Mortal Wkly Rep CDC Surveill Summ 1996. analgesics.177 articular or extra-articular subtalar fusion. Smith BP. Yeargin-Allsopp M. Etiologic factors in cerebral palsy. lengthening of the gastrocnemius aponeurosis alone. Willoughby RE. et al. du MC. Nelson KB. Trends in mortality and cerebral palsy in a geographically based cohort of very low birth weight neonates born between 1982 to 1994. 5: 11–23. Dev Med Child Neurol 1998. Sensibility deficiencies in the hands of children with spastic hemiplegia. 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 Conclusion The management of patients with cerebral palsy continues to evolve. including the technical success of surgical procedures. Holmgreen P. 9: 81–88. improve function. Elliott M. Development of bladder control in children and adolescents with cerebral palsy.180 Rotational or torsional deformities can be managed by rotational osteotomy of the tibia. recurrence of this deformity is possible in children who undergo surgery before they are 10 years old. Van Heest AE. Cerebral palsy.185 Medial and lateral hamstring lengthening combined with psoas lengthening decreases pelvic tilt. Dev Med Child Neurol 2001. Evans P. Arch Dis Child 2002. Doernberg NS. fibula. hallux valgus.190 Onestage comprehensive hip reconstruction is an effective treatment for children aged 4 years or older who have a migration index greater than 60%. O’Shea TM. Hagberg G. Life expectancy of adults with cerebral palsy. hip subluxation with scissoring is initially managed by: adductor tenotomy alone. Coene S. Dillard RG. control of movement disorders and deformity. Pediatr Ann 1986. Pharoah PO. and anterior branch obturator neurectomy—are most effective in patients with stable hips without bony deformity. Only reproduce with permission from The Lancet. Preisser JS. 13: 133–39. Boyle CA. or femur to correct foot progression angle. Rosenbaum P. Kennes J. Stanley E.com For personal use. Int J Epidemiol 1992. De Rammelaere M. inflammation and the risk of cerebral palsy. Surgical procedures of the hip are designed to improve abduction (decrease scissoring). Vanderkelen R. functional status. or total joint replacement if nonoperative management (anti-inflammatory dugs. Roijen LE. 15: 191. Nelson KB. Hutton JL. 44: 370–82.187 combined adductor tenotomy and iliopsoas lengthening. and improve self-esteem in these patients.174.181 Knee joint contractures require capsulotomy182 and associated.189 In older children. 26: 137–45. Neuroimpairments. Decoufle P. inappropriate coexisting contraction of the rectus femoris might require release or transfer of the rectus femoris to the iliotibial band or a medial hamstring. Prevalence and time trends of disabilities in school-age children. the development of techniques to strengthen and improve motor power. Surveillance of cerebral palsy in Europe: a collaboration of cerebral palsy surveys and registers. hindfoot valgus. Vanneste G. activity limitations. 21: 359–66. N Engl J Med 1994. Paediatr Drugs 2003.SEMINAR The most commonly reported procedures used to correct equinus ankle and foot deformity include lengthening of the Achilles tendon. How common are the cerebral palsies? In: Cerebral palsies: epidemiology and causal pathways.190 The Reimer’s migration index describes the amount of the femoral head that is subluxated out of the acetabulum expressed as a percentage. Postema K. Paneth N. 43: 103–07. Lipton GE. Spasticity associated with cerebral palsy in children: guidelines for the use of botulinum A toxin. positively affect health-related quality of life. Limbeek VJ. Dev Med Child Neurol 2002. Mlika A. J Hand Surg [Am] 1993.186 Many non-ambulatory patients with cerebral palsy are characterised by hip instability that is associated with hip pain and difficulties with walking and sitting. Hanna SE. Motor disability in children in three birth cohorts. instruments that can be used to assess multiple outcomes of various therapeutic options. 2000: 22–39. Pediatrics 1994. The availability of validated and reliable outcome 22 1628 THE LANCET • Vol 363 • May 15. and the identification of surgical procedures to correct deformities will provide resources that can be used to modify untoward natural histories. to prevent hip subluxation. Causes of cerebral palsy. Alberman E. 1991. Schendel DE. Dev Med Child Neurol 2000.70. Effects of cognitive. Koman LA.thelancet. 11: 487–91. Dequae L. House J. transfer of the Achilles tendon. 60: 940–45. Prevalence of selected developmental disabilities in children 3-10 years of age: the Metropolitan Atlanta Developmental Disabilities Surveillance Program. 2004 • www. will facilitate the appropriate evaluation of the interventions currently used to manage children and adults with cerebral palsy. Refractory valgus deformity can be corrected by: medial displacement osteotomy of the calcaneus. Curr Opin Pediatr 1999. Cerebral palsy in multifoetal pregnancies. Varus deformity can be managed by tendon lengthening. and participation restrictions in children with cerebral palsy.174. Surgical options to treat painful dislocated hips include resection of the femoral head. Arch Dis Child 1985. or to restore hip joint congruency. adductor transfer. Crouched gait and knee flexion deformities are corrected by medial or combined medial and lateral hamstring lengthening procedures. Dev Med Child Neurol 2002. 330: 188–95. Boyle CA. anti-inflammatory drugs. References 1 2 Kuban KC. Current management models are patient-centred and are focused on modification of spasticity. 45: 1–14. or calcaneal osteotomy. Evans S. London: MacKeith Press. Kuppevelt VH. 197–201. iliopsoas release or recession. The availability of oral and parenteral drugs. Blickstein I.188 or less commonly. 101: 642–47. Putnam M. abduction osteotomy of the proximal femur. Stiers P. Cans C. the ability to alter spasticity with surgical procedures.179 or triple arthrodesis. Infection. 44: 352–55. Klinepeter KL.176. however.184 Proximal hamstring lengthening is effective in the treatment of knee deformities in nonambulatory children. . Dev Med Child Neurol 2002. motor. health-related quality of life. 44: 309–16. Strauss D. Yeargin-Allsopp M. Visual-perceptual impairment in a random sample of children with cerebral palsy. or antispasticity medications). Leviton A. Femoral osteotomy can improve hip coverage during stance. Soft-tissue procedures—adductor tenotomy. Shavelle R. 93: 399–403. and utility. 86: 84–89. Miller F.

39 Stanley FJ. Only reproduce with permission from The Lancet. Leverin AL. Goodman A. Volpe JJ. Curr Opin Pediatr 2000. J Neurosci 2001. Infection in pregnancy and cerebral palsy. Botulinum toxin A as an alternative to serial casting in the conservative management of equinus in cerebral palsy. Improved scaling of the gross motor function measure for children with cerebral palsy: evidence of reliability and validity. Phys Ther 2000. 47 Russell DJ. Coleman G. Ware JE. Levine JM. et al. 35 Ingram TTS. Byrt TA. 63 Landgraf JM. 44: 447–60. 38 Pharoah PO. 43 Msall ME. 43: 4–15. 36 Bleck EE. 21: 1302–12. The gross motor performance measure: validity and responsiveness of a measure of quality of movement. J Bone Joint Surg 1981. 80: 974–85. Role of the fetus in perinatal infection and neonatal brain damage. prevalence and origin during the birth year period 1983–1986. Moskowitz C. Pediatrics 2003. Gaebler-Spira DJ. 72 Butler C. Birthweight specific trends in cerebral palsy. Interrater reliability of a modified Ashworth scale of muscle spasticity. Health-related quality of life outcomes measures. 60 Barry MJ. et al. 1984: 1–12. Randomized controlled trial of physiotherapy in 56 children with cerebral palsy followed for 18 months. Hu X. Phys Ther 1990. Corry IS. McLellan DL. 31 Schendel DE. 43: 778–90. et al. 37 Hagberg B. 57 Tardieu G. Gowland C. Dev Med Child Neurol 1995. Goldberg MJ. Mooney JF III. The Functional Independence Measure for Children (WeeFIM): conceptual basis and pilot use in children with developmental disabilities. 119: 241–44. Lobb GL. Barron R. 28 Foster-Barber A. Torrance GW. et al. 29 Gaudet LM. 16: 16–23. Dev Med Child Neurol 2001. 33 Sanger TD. Validation of a model of gross motor function for children with cerebral palsy. Neurology 1985. Romanko MJ. 75: 603–13. 67: 206–07. Hagberg G. Bacterial endotoxin sensitizes the immature brain to hypoxic–ischaemic injury. 82: 387–93. Oleari G. Duffy CM. Graham HK. Silberstein CE. Coryell J. 33: 375–84. Zucman E. Alberman. Rosenbaum PL. 70: 602–10. Seid M. Surgery 1996. 56: 105–08. J Child Neurol 2001. Dev Neurosci 2001. Fahn S. 33: 421–30. J South Orthop Assoc 2003. Law M. Arch Phys Med Rehabil 2000. Watson L. Smith MB. . Burnett M. Sponseller PD.SEMINAR 23 Flett PJ. 68 O’Brien CF. 30 Ness JK. Barr RD. A dynamic approach to the thumb-in-palm deformity in cerebral palsy. 13: 1101–06. Arch Dis Child 1990. Dev Med Child Neurol 2003. et al. J Pediatr Orthop 1994. Levison SW. VanSwearingen JM. Fidler MO. Shentoub S. Eur J Neurol 1999. Spasticity management: an overview. Delarue R. Dev Med Child Neurol 2003. Raina PS. validity. Neurologique 1954. Evaluation of the functional effects of a course of Bobath therapy in children with cerebral palsy: a preliminary study. Cooke T. In: Stanley F. 42 Feldman AB. McLeod RS. Clin Pediatr 1994. PedsQL 4. 12: 369–80. McMaster University. Lossing A. Human perinatal asphyxia: correlation of neonatal cytokines with MRI and outcome. double-blind trial. J Am Med Womens Assoc 2001. Dev Med Child Neurol 2002. Orthopaedic management in cerebral palsy. Wachtel RC. 63A: 216–25. 111: e89–e97 (abstr). 69 Graham HK. 52 Koman LA. 49 Palisano RJ. 2002. Delgado MR. Russell D. Gurucharri LM. Catanese T. Bach TM. Palisano RJ. 1996–2001. Development of a clinical assessment of quality of movement for unilateral upper-limb function. Classification and definition of disorders causing hypertonia in childhood. 51 Cosgrove AP. Rosenbloom L. 81 (suppl 2): S30–45. 36: 386–96. Hanna SE. Validity and reliability of a rating scale for the primary torsion dystonias. Physiotherapy 1969. Dev Med Child Neurol 1998. Mallard C. QUEST Quality of Upper Extremity Skills Test Manual. Friedman J. Kurtin PS. Philadelphia: JB Lippincott. Randall MJ. Measurement in surgical clinical research. 24 Essex C. 45: 85–91. Campbell MJ. 32 Goldstein EM. Dev Med Child Neurol 1994. Gutierrez AL. 64 Daltroy LH. 53 Mackey AH. 318: 803–08. Pagliano E. Delacato C. Reliability and validity of the Observational Gait Scale in children with spastic diplegia. 25 Back SA. Phys Ther 2000. Efficacy of programmes based on conductive education for young children with cerebral palsy. 66 Schneider JW. 56 Bohannon RW. Kinney HC. Helders PJ.thelancet. Rogers BT. The Child Health Questionnaire user’s manual. Med Care 2001. 75 Bobath B. Recurrence of equinus foot deformity in cerebral palsy patients following surgery: a review. 91: 143–44. 34 Fedrizzi E. Andreucci E. 12: 1–9. 76 Knox V. 73 Palmer FB. Objective measurement of clinical findings in the use of botulinum toxin type A for the management of children with cerebral palsy. Smith GN. Reliability and responsiveness of the Barry-Albright Dystonia Scale. 35: 73–77. Acta Paediatr 1993. 39: 6–14. Ann Med 2001. 56: 433–36. Shapiro BK.0: reliability and validity of the Pediatric Quality of Life Inventory version 4. JAMA 1960. The treatment of neuromuscular disorders by improving patterns of co-ordination. The POSNA pediatric musculoskeletal functional health questionnaire: report on reliability. 45 DeMatteo C. Phys Ther 1987. 77 Doman RJ. The Health Institute. 59 Burke RE. Liang MH. Dev Med Child Neurol 2001. Rothstein RP. BMJ 1992. The Health Utilities Index (HUI) system for assessing health-related quality of life in clinical studies. Oke LE. 44 Johnson LM.com 1629 For personal use. Feeny DH. Clin Rehabil 1998. 71 Bower E. Trends in perinatal mortality and cerebral palsy in Western Australia. Perinatal hypoxia-ischemia induces apoptotic and excitotoxic death of periventricular white matter oligodendrocyte progenitors. 174: 257–62. 55 Ashworth B. Phys Ther 1995. 80: 873–85. Harryman SE. 36: 965–73. randomized. Dev Med Child Neurol 1999. Taylor NF. Wood TL. Marsden CD.0 generic core scales in healthy and patient populations. Neurodevelopmental Research Unit. 70 Koman LA. 1st edn. Olow I. Concurrent and construct validity of the Pediatric Evaluation of Disability Inventory. King J. Children with severe brain injuries: neurological organization in terms of mobility. Mulvaney T. Treatment of spasticity with botulinum toxin. Hadley-Miller NA. Ontario: Central West Health Planning Information Network. 43: 601–08. Meyers AR. Luo NL. Obstet Gynecol Surv 2001. Doman G. 65: 602–06. Bressman SB. 62 Wright JG. 78 Reddihough DS. 41: 404–11. 39: 800–12. Walter S. Horseback riding in THE LANCET • Vol 363 • May 15. Graham HK. Cooke RW. 55: 18–22. Canada: 1992. N Engl J Med 1988. Management of spasticity in cerebral palsy with botulinum-A toxin: report of a preliminary. 50 Corry IS. 67 Furlong WJ. Evans AL. et al. Aoki KR. Vokes DA. 192: 540–42. 44: 68–72. France AP. Rosenbaum P. Pollock N. Reddihough DS. 45: 213–15. Abetz I. J Paediatr Child Health 2003. A historical view of the definition and classification of the cerebral palsies. Cosgrove AP. Darrah J. Late oligodendrocyte progenitors coincide with the developmental window of vulnerability for human perinatal white matter injury. Dev Med Child Neurol 2001. 304: 1658–67. Rosenbaum PL. Gait Posture 2000. 48 Boyce WF. 74 Damiano DL. Michell D. and sensitivity to change. 61 Andresen EM. Ferriero DM. DiGaudio K. Atkins EA. J Pediatr Orthop 1998. Vermeer A. 18 (suppl): S182–90. 26 Dammann O. Smith BP. Walt SE. Haley SM. 58 Boyd RN. Preliminary trial of carisoprodol in multiple sclerosis. 40 An evaluation of cerebral palsy data for epidemological studies: Ontario. Gaebler-Spira D. Albright AL. Autti-Rämö I. 2004 • www. Hand function in children with hemiplegic cerebral palsy: prospective follow-up and functional outcome in adolescence. Practitioner 1964. Mink JW. Avery LM. Health-related quality of life and functional outcome measures for children with cerebral palsy. Comparing reliability and validity of pediatric instruments for measuring health and well-being of children with spastic cerebral palsy. 23: 213–18. Functional motor abilities of children with cerebral palsy: a systematic literature review of assessment measures. Fossel AH. Hyperbaric oxygen and cerebral palsy: no proven benefit and potentially harmful. Dev Med Child Neurol 2002. New England Medical Center: 1996. Dev Med Child Neurol 1994. Clin J Pain 2002. Rogers BT. 27 Eklind S. Recommendations for the use of botulinum toxin type A in the management of cerebral palsy. Walter SD. 18: 561–71. Rehabilitation of spasticity and related problems in childhood cerebral palsy. Dev Neurosci 2001. Botulinum toxin in the management of the lower limb in cerebral palsy. Philadelphia: JB Lippincott. Borenstein NS. 79 Sterba JA. Effects of neurodevelopmental treatment (NDT) for cerebral palsy: an AACPDM evidence report. 6: S23–35. eds. Cerebral palsy and chorioamnionitis: the inflammatory cytokine link. Stott NS. 44: 468–76. Smith BP. A la recherche d’une technique de mesure de la spasticité. 41 McCarthy ML. Eur J Neurosci 2001. The changing panorama of cerebral palsy in Sweden: VI. Should we be testing and training muscle strength in cerebral palsy? Dev Med Child Neurol 2002. Walters BC. Spitz EB. Dickens B. Dev Med Child Neurol 2003. Rosenbaum PL. 11: 67–79. 23: 203–08. Dodd K. The epidemiology of the cerebral palsies. 54 Ketelaar M. 12: 99–104. Gwathmey FW. 14: 299–303. 65 Varni JW. 1987. 45: 4–11. Leviton A. Hallett M. The effects of physical therapy on cerebral palsy: a controlled trial in infants with spastic diplegia. 37: 20–21. 40: 763–70. 46 House JH.

MacKay-Lyons M. et al. Al Dabbagh Z. Thomas SS. Schaumburg SW. Mooney JF. Neurosci Behav Physiol 1997. Sussman M. Arch Phys Med Rehabil 1964. Gershkoff AM. Botulinum toxin treatment of spasticity in diplegic cerebral palsy: a randomized. Smith BP. Stern LM. Reconstr Surg Traumatol 1972. Berg K. Rang M. 96: 50–51. Van Den Bergh PY. Hyperbaric oxygen for children with cerebral palsy: a randomised multicentre trial. Dev Med Child Neurol 2002. 44: 436–46. McClean D. Parrott J. Green NE. J Pediatr Orthop 1998. Jahnke MT. Connell TM. 85 Taub E. Ward C. Mubarak SJ. 94 Hesse S. 10: 1–9. Lavinder G. 102 Montgomery D. Botulinum toxin A compared with stretching casts in the treatment of spastic equinus: a randomised prospective trial. J Child Neurol 1996. 44: 364–69. Waddy H. The use of open phenol blocks to the motor branches of the tibial nerve in adult acquired spasticity. 108 Mooney V. 77A: 1590–606. A randomized study of combined botulinum toxin type A and casting in the ambulant child with cerebral palsy using objective outcome measures. Siebel A. Mulvaney T. J Child Neurol 2001. 87 Pierce SR. Moor M. Yamashita T. 40: 176–81 81 Barry MJ. 16: 113–18. Dev Med Child Neurol 2001. 30: 120–24. Botulinum toxin as a biological weapon: medical and public health management. Herzog R. 125 Wissel J. 101 Collet JP. Int J Lang Commun Disord 1998. 106 Mason C. 103 Hardy P. Arch Dis Child 2000. 13: 18–36. 63: 122–31. 121 Koman LA. 122 Sutherland DH. et al. 26: 235–42. The effect of botulinum toxin type A and a variable hip abduction orthosis on gross motor function: a randomized controlled trial. Severa S. Schenkel A. Foot Ankle 1991. 4: 164–66. Goodman A. 86 Crocker MD. Brace treatment in neuromuscular spine deformity. Bennett JT. Amar M. Frykman G. Pedersen SA. Forced use of the upper extremity in cerebral palsy: a single-case design. 104 Albright AL. Jonkers I.com For personal use. 13: 68–76. Allgar V. Dev Med Child Neurol 1997. Therapeutic electrical stimulation in cerebral palsy: a randomized. Dev Med Child Neurol 1998. Dev Med Child Neurol 2001. 83: 481–87. Tardieu C. Roussounis SH. Botulinum toxin A in the hemiplegic upper limb: a double-blind trial. 93 Scheker LR. 44: 666–75. 117 Gormley ME. 23: 82–85. Wyatt MP. Ives HL. Inglesby TV. 96 Crenshaw S. McDonnell E.thelancet. 90 Carmick J. 83: 1462–63. 129 Desloovere K. Daly K. 127 Corry IS. Dev Med Child Neurol 2001. Collet JP. Neuropediatrics 1999. Double-blind comparison study of two doses of botulinum toxin A injected into calf muscles in children with hemiplegic cerebral palsy. Rosenfeld S. Basis for a method of dynamic proprioceptive correction in the restorative treatment of patients with residual-stage infantile cerebral palsy. 118 Baker R. Goldberg J. Use of botulinum toxin type A in pediatric patients with cerebral palsy: a three-center retrospective chart review. Botulinum toxin type A neuromuscular blockade in the treatment of lower extremity spasticity in cerebral palsy: a randomized. Cosgrove AP. Mov Disord 2002. 8 (suppl 5): 75–87. Gait Posture 1999. Brashear A. 17: 162–69. Steele C. Luecke D. Griffin PP. 123 Ubhi T. et al. Hariga J. Temple T. Castagno P. J Pediatr Orthop 1992. 131 Boyd RN. et al. Leon JM. J Pediatr Orthop 2000. Goldberg J. et al. Boulton JE. 45: 513–19. 80 Hutzler Y. Ramirez S. Pediatr Neurosurg 1995. 95 Buckon CE. 22: 497–501. Molenaers G. 12: 470–74. Walsh EG. 13: 628–33. placebo-controlled trial. Gallagher KG. 19: 376–79. 73: 505–13. JAMA 2001. . Phys Ther 1993. Neuromuscular approach to the motor deficits of cerebral palsy: a pilot study. Markestad T. 113 Tardieu G. J Bone Joint Surg 1995. et al. Wallace WA. et al. J Pediatr Orthop 1999. Dev Med Child Neurol 1980. Intrathecal baclofen in cerebral palsy movement disorders. Aiona M. Dev Med Child Neurol 2002. Dev Med Child Neurol 2002. Davie A. 24: 226–32. 92 Sommerfelt K. Vanasse M. J Pediatr 2000. Morello A. 111 Carpenter EB. Neurosci Lett 1995. 3: 279–86. Hansen FJ. et al. 116 Bakheit AM. Chesher SP. 44: 301–08. et al. Morris DM. 105 Albright AL. An evaluation of botulinum-A toxin injections to improve upper extremity function in children with hemiplegic cerebral palsy. White MA. Renders A. 11: S51–60. 132 Koman LA. Bergman U. Janosky J. placebo-controlled clinical trial. et al. Role of nerve blocks in the foot and ankle in cerebral palsy: therapeutic and diagnostic. Nichol B. Cerebral palsy: orthopaedic management. Smith B. 11 (suppl 1): S29–35. Eur J Neurol 2001. Seeger JD.SEMINAR children with cerebral palsy: effect on gross motor function. Lancet 2001. Cosgrove A. 43: 371–78. 33 (suppl): 24–25. crossover trial. 13: 489–95. Clin Orthop Rel Res 1969. 16: 332–35. Hariga J. Rossiter D. Dev Med Child Neurol 2000. Jasinski M. dose-ranging study. Nurs Times 2000. Bhakta BB. 88 Willis JK. 137: 331–37. Taylor TC. J Pediatr Orthop 1996. Chipman M. Glazier J. 98 Letts M. Gordon AM. Mauritz KH. 2004 • www. Chacham A. Effects of a movement and swimming program on vital capacity and water orientation skills of children with cerebral palsy. 107 Khalili AA. Szeinberg A. 82 Stewart K. Barry MJ. Cosgrove AP. the roots by the epidural route. The effect of intrathecal baclofen on functional intelligibility of speech. Rice JC. Benton JG. or of the posterior tibial nerve: their indications and contra-indications in the various forms of spasticity (experience of 10 years)] Rev Neurol (Paris) 1971. et al. Physical therapy interventions for patients with movement disorders due to cerebral palsy. Neuromuscular electrical stimulation and dynamic bracing as a treatment for upper-extremity spasticity in children with cerebral palsy. Effects of hyperbaric oxygen therapy on children with spastic diplegic cerebral palsy: a pilot project. 43: 234–38. Selective partial denervation by alcohol injections and their results in spasticity. 285: 1059–70. Lejeune TM. Heinen F. 20: 108–15. Comparison of three ankle-foot orthosis configurations for children with spastic hemiplegia. Intramuscular alcohol as an aid in management of spastic cerebral palsy. 89 Pape KE. 112 Tardieu G. Duffy CM. Soft Boston orthosis in management of neuromuscular scoliosis: a preliminary report. J Pediatr Orthop 1993. Am J Occup Ther 1997. Pediatr Phys Ther 2001. Botulinum toxin type A 1630 THE LANCET • Vol 363 • May 15. Randomised double blind placebo controlled trial of the effect of botulinum toxin on walking in cerebral palsy. Safety profile and efficacy of botulinum toxin A (Dysport) in children with muscle spasticity. 120 Corry IS. Maciag-Tymecka I. double-blind study of “high-dose” versus “low-dose” treatment. Boyd R. J Pediatr Orthop 1993. 110 Carpenter EB. Undersea Hyperb Med 1999. placebo-controlled. 27: 639–43. Arch Phys Med Rehabil 2002. Forster S. et al. 8 (suppl 5): 109–19. 357: 582–86. McGowan S. 42: 116–21. Rathbone D. Management of cerebral palsy with botulinum-A toxin: preliminary investigation. controlled. 44: 551–55. 18: 304–11. Graham HK. Gibson SK. Root L. Saetesdal I. 97 Miller A. 201: 37–40. Analgesic effects of botulinum toxin A: a randomized. Kaufman KR. Galil A. III. Short-term electrical stimulation enhances the effectiveness of Botulinum toxin in the treatment of lower limb spasticity in hemiparetic patients. Harmel MH. Dev Med Child Neurol 2002. 119 Barwood S. Tardieu C. Botulinum toxin and short-term electrical stimulation in the treatment of equinus in cerebral palsy. Double-blind study of botulinum A toxin injections into the gastrocnemius muscle in patients with cerebral palsy. Threshold electrical stimulation (TES) in ambulant children with CP: a randomized double-blind placebo-controlled clinical trial. Constraint-induced therapy for a child with hemiplegic cerebral palsy: a case report. doubleblind. Doderlein L. 99 Olafsson Y. Morton R. Eur J Neurol 2001. Mooney JF. 126 Polak F. Dev Med Child Neurol 2002. Dobson F. 91 Dali C. Management of spasticity by selective peripheral nerve block with dilute phenol solutions in clinical rehabilitation. 130 Detrembleur C. McNeill S. 128 Flett PJ. III. Ballieu C. Curr Atheroscler Rep 2001. The efficacy of tone-reducing features in orthotics on the gait of children with spastic diplegic cerebral palsy. Effects of continuous intrathecal baclofen infusion and selective posterior rhizotomy on upper extremity spasticity. Schechter R. Gaebler-Spira D. Keeler A. J Pediatr Orthop 2000. et al. J Child Neurol 1996. Only reproduce with permission from The Lancet. Jakobson-Huston S. Saraste H. 84 Charles J. 39: 185–93. Anderson RB. 20: 210–16. 109 Moore TJ. 125: 63–68. 11: 219–21. Foot Ankle 1983. Chambers HG. 110: 94–96. Fasick MP. Current status of intraneural phenol injections. Forced use treatment of childhood hemiparesis. Constraint-induced movement therapy to enhance recovery after stroke. double-blind. Massage for children with cerebral palsy. 124 Fehlings D. [Infiltrations with 45 degrees ethyl alcohol of the motor points. Kirsch SE. 114 Arnon SS. Seitz DG. 115 Koman LA. Neuropsychological effects of hyperbaric oxygen therapy in cerebral palsy. Effects of constraint-induced therapy on hand function in children with hemiplegic cerebral palsy. Gilpin P. part 1. Walker F. 51: 824–33. Graham HK. Delgado MR. 100 Renshaw TS. Botulinum toxin A in the management of spastic gait disorders in children and young adults with cerebral palsy: a randomized. 35: 71–77. Pediatrics 2002. Marois P. McLamb J. Botulinum toxin A versus fixed cast stretching for dynamic calf tightness in cerebral palsy. 43: 609–13. Clinical use of neuromuscular electrical stimulation for children with cerebral palsy. 83 Semenova KA. Miller F. J Paediatr Child Health 1999. J Hand Surg [Br] 1999. Impact of orthoses on the rate of scoliosis progression in children with cerebral palsy.

164 Strecker WB. Graham HK. Sathy M. Wang T. Surgical reconstruction of the upper extremity in cerebral palsy. 154 Manske PR.com 1631 For personal use. 11: 494–97. Albarracin JP. J Neurosurg 1997. Albrecht MM. 136 Peacock WJ. Griffin PP. 157 Koman LA. Trost JP. Upper extremity tendon transfers in cerebral palsy: electromyographic and functional analysis. Owen JH. Zimbler S. 160: 509–12. 31: 665–69. J Bone Joint Surg Br 2001. J Hand Surg 1999. Eastman RW. Eur J Pediatr 2001. Sarwark JF. Cochrane DD. Management of hip disorders in patients with cerebral palsy. 18: 703–11. Clin Orthop 1990. Hip adductor transfer compared with adductor tenotomy in cerebral palsy. Kestle J. 111: 874–76. 177 Mosca VS. 176 Andreacchio A. S Afr Med J 1981. 145 Graham HK. Sutherland D. Lauder AJ. 87: 1001–03. 190 Flynn JM. J Bone Joint Surg Am 1995. Wenger DR. Cardelia JM. Skaggs D. J Hand Surg [Br] 1999. Scoliosis in the institutionalized cerebral palsy population. 179 Drvaric DM. Standards in anterior spine surgery in pediatric patients with neuromuscular scoliosis. Millis MB. The stability of the hip in children: a radiological study of the results of muscle surgery in cerebral palsy. J Pediatr Orthop 1991. 141 Chicoine MR. 134 Jongerius PH. Clin Orthop 1999. et al. 187Cottalorda J. Miller F. 36: 133–41. Birnbaum R. Progression of scoliosis in spastic quadriplegic patients after the insertion of an intrathecal baclofen pump. 161 Gu Y. 2004 • www. Poehling GG. Operative treatment of cerebral palsy. 22: 158–64. 169 Mowery CA. J Pediatr Orthop 2001. Treatment of knee contracture in cerebral palsy by hamstring lengthening. 70A: 1290–96. 20: 501–05. 83: 364–70. J Hand Surg 1988. Prediction of outcome after rectus femoris surgery in cerebral palsy: the role of cocontraction of the rectus femoris and vastus lateralis. 133 Wong V. Am J Orthop 1997. Hand Clin 1990. Calcaneal lengthening for valgus deformity of the hindfoot: results in children who had severe. Sutherland DH. J Bone Joint Surg Br 2001. Outcome of medial versus combined medial and lateral hamstring lengthening surgery in cerebral palsy. DeLuca PA. Ounpuu S. Gelberman RH. Dabney KW. 160 Mittal S. 143 Boscarino LF. 173 Doute DA. Anterior elbow release of spastic elbow flexion deformity in children with cerebral palsy. Orthop Clin North Am 1988. N Engl J Med 1992. J Bone Joint Surg 1976. Armstrong RW. 163 Manske PR. 83: 259–62. Proximal hamstring lengthening in the sitting cerebral palsy patient. 10: 300–09. 4. 178 Alman BA. Walker K. Cerebral palsy of the upper extremity. Dev Med Child Neurol 2002. 171 Matev I. Rotteveel JJ. 165 Van Heest AE. Goldner RD. Clin Orthop 1990. Phillips LH II. 185 Elmer EB. Schutte L. 186 DeLuca PA. Hand Clin 1988. Isolated calf lengthening in cerebral palsy: outcome analysis of risk factors. Kaufman BA. Shen L. Ounpuu S. Pediatr Neurol 1998. 13: 180–83. 138 Park TS. 13: 634–41. Lengthening of the calcaneal tendon in spastic hemiplegia by the White slide technique. 150 Thometz JG. 253: 75–89. 13A: 540–43. Gage JR. 1: 525–43. 148 Thomson JD. Lateral column lengthening as treatment for planovalgus foot deformity in ambulatory children with spastic cerebral palsy. Allen BL Jr. 159 Cooper J. 175 Koman LA. Cardoso DR. Simon SR. Mooney JF3. J Pediatr Orthop 2002. J Hand Surg [Br] 1991. J Pediatr Orthop 2000. J Hand Surg 1999. 152 Ginsberg GM. Charmet E. Vogler GP. Cariello C. 162 Goldner JL. Farmer JP. Castagno P. J Child Neurol 1995. 86: 34–39. Fixsen JA. Only reproduce with permission from The Lancet. 77: 500–12. Predicting the outcome of adductor tenotomy. Gelberman R. 364: 48–52. House JH. 167 Pinzur MS. posterior capsulotomy. . Surgical management of spastic diplegia in cerebral palsy. 188 Novacheck TF. 174 Fulford GE. J Hand Surg 1986. Goldschmidt RB. 20: 43–49. Pediatr Neurosurg 1994. 144 Mooney JF. 183 Chambers H. Al Atassi B. The neurosurgical management of spasticity. Craig CL. 22: 169–72. Mitani M. 24A: 323–30. S Afr Med J 1997. Adolfsson L. Metton G. 166 El Said NS. Dietz FR. Kaufman K. Dev Med Child Neurol 1989. III. Miller F. 146 Reimers J. et al. Lipton GE. 26: 613–16. J Pediatr Orthop 1993. 153 Van Heest AE. 21: 756–60. J Bone Joint Surg 1988. Cadaveric modeling of the pronator teres rerouting tendon transfer. Stark HH. 6: 583–89. 184: 1–100. 149 Ferguson RL. et al. Schwartz MH. Impact of selective posterior rhizotomy on fine motor skills: long-term results using a validated evaluative measure. Chin Med J (Engl) 1998. 151 Sarwahi V. Nakano JM. Schmitt EW. 19: 419–25. Effects of selective dorsal rhizotomy for spastic diplegia on hip migration in cerebral palsy. Chavrier Y. Long-term follow-up on tendon transfers to the extensors of the wrist and fingers in patients with cerebral palsy.5 year follow-up after surgical correction of upper extremity deformities in spastic cerebral palsy. open-label clinical trial. Boyes JH. Davis RB. 184 Miller F. 253: 55–61. Walsh JH. 182 Beals RK. et al. 44: 17–25. Rethlefsen SA. Spine 1981.thelancet. Rapid progression of hip subluxation in cerebral palsy after selective posterior rhizotomy. Mubarak SJ. Use of botulinum toxin injection in 17 children with spastic cerebral palsy. Spero CR. Spinal deformity after selective dorsal rhizotomy in patients with cerebral palsy. 189 Root L. A randomized clinical trial to compare selective posterior rhizotomy plus physiotherapy with physiotherapy alone in children with spastic diplegic cerebral palsy. 10: 6–9. van Hulst K. management of the upper extremity. Orellana CA. and quadriceps mechanism shortening. J Am Acad Orthop Surg 2002. Gautheron V. J Pediatr Orthop 1985. 21: 772–77. 253: 62–74. Intramuscular psoas lengthening improves dynamic hip function in children with cerebral palsy. Pediatr Neurosurg 2002. 24: 614–18. 140 McLaughlin J. 180 Green NE. J Pediatr Orthop 2001. J Pediatr Orthop 1998. Joosten F. Gelberman RH. 108: 1062–71. Davis RB. J Hand Surg [Br] 1991. 44 (suppl 91): 13–14. Dailey L. 168 Hoffer MM. III. 13: 174–79. Clin Orthop 1990. Acta Orthop Scand Suppl 1980. The Grice extra-articular subtalar arthrodesis in the treatment of spastic hindfoot valgus deformity. Manske PR. Strecker WB. Selective dorsal rhizotomy and rates of orthopedic surgery in children with spastic cerebral palsy. 326: 745–49. Banta JV. J Pediatr Orthop 1997. Flexor origin release and functional prehension in adult spastic hand deformity. 18: 712–18. Gross RH. Subtalar arthrodesis for stabilization of valgus hindfoot in patients with cerebral palsy. Silberstein CE. THE LANCET • Vol 363 • May 15. Shiavi R. Surgery of the spastic thumb-in-palm deformity. Toby BE. Selective dorsal rhizotomy: meta-analysis of three randomized controlled trials. Koman LA. van den Hoogen F. Considerations in the treatment of cerebral palsy patients with spinal deformities. Lehman M. 147 Madigan RR. Rosenblatt B. Split posterior tibial-tendon transfer in spastic cerebral palsy. 70B: 472–75. 172 Borton DC. 17: 603–07. 156 Szabo RM. J Bone Joint Surg Am 1983. Nattrass GR. Scoliosis in cerebral palsy: an overview and recent results.SEMINAR neuromuscular blockade in the treatment of equinus foot deformity in cerebral palsy: a multicenter. J Pediatr Orthop 1993. 12: 329–36. 63: 767–72. Reiner AM. Leet A. 158 Goldner JL. Bjornson K. 39: 178–84. 4: 223–65. Dev Med Child Neurol 2002. Hand Clin 1985. J Pediatr Orthop 1998. Dev Med Child Neurol 1997. Temkin N. 135 Arens LJ. 16: 133–36. Effects of selective dorsal rhizotomy on gait in children with cerebral palsy. J Pediatr Orthop 2002. J Bone Joint Surg 1988. 22: 374–79. Selective release of the flexor origin with transfer of flexor carpi ulnaris in cerebral palsy. Int Orthop 1998. Surgical management of ankle and foot deformities in cerebral palsy. J Pediatr Orthop B 2001. 170 Filler BC. 139 Steinbok P. symptomatic flatfoot and skewfoot. Experience with botulinum toxin in the treatment of cerebral palsy. Goodman A. Capsulodesis of the metacarpophalangeal joint of the thumb in children with cerebral palsy. 137 Park TS. The determination of sensory deficits in children with hemiplegic cerebral palsy. Comparison of pronator tenotomy and pronator rerouting in children with spastic cerebral palsy. Pediatrics 2001. Management of valgus hindfoot deformity in pediatric cerebral palsy patients by medial displacement osteotomy. Miller F. Atkins E. Langewisch KR. Goldberg MJ. Arthrodesis of the metacarpophalangeal joint of the thumb in children and adults: adjunctive treatment of thumb-in-palm deformity in cerebral palsy. Effect of hamstring and psoas lengthening on pelvic tilt in patients with spastic diplegic cerebral palsy. J Bone Joint Surg Am 1981. The effect of rectus EMG patterns on the outcome of rectus femoris transfers. Beauchamp R. 142 Greene WB. 5: 69–72. Lauer A. J Pediatr Orthop 1993. 24: 719–23. 16: 127–32. 65: 748–54. 43: 802–05. Cai P. Maatougui K. Dev Med Child Neurol 2001. J Pediatr Orthop 1992. Division of C8 nerve root for treatment of spastic cerebral palsy in the upper limbs: a preliminary report. Upper extremity surgical treatment of cerebral palsy. Sponseller PD. Majnemer A. Cerebral palsy. Wallace SL. 60: 849–50. Gelberman RH. Rhoades CE. Carlstrom C. 58A: 667–70. Soleus neurectomy for dynamic ankle equinus in children with cerebral palsy. 6: 697–709. Sussman MD. 18: 124–31. Schafer MF. Emanuel JP. Gabreels FJ. 181 Kay RM. Levin S. 11A: 836–40. Bowen TR. Leary PM. Progression of scoliosis after skeletal maturity in institutionalized adults who have cerebral palsy. Pirpiris M. Botulinum toxin A: a new option for treatment of drooling in children with cerebral palsy: presentation of a case series. Park TS. 10: 198–209. Tolo VT. 155 Nylander G.

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