Cerebral Palsy: An Overview


  • Koza Duman

Received Date: 22.11.2021 Accepted Date: 20.12.2021 Hamidiye Med J 2022;3(1):1-6

Cerebral palsy (CP), the most common cause of disability in childhood, was first described in 1861 by the English orthopedist William Little. CP, which has been expressed in different forms for many years, has been defined in 2006 by an international consensus as “a group of permanent disorders of the development of movement and posture, causing activity limitation that are attributed to non-progressive disturbances that occurred in the developing or fetal brain”. CP still remains the most common cause of childhood disability with a prevalence of 1.7-3.1 per 1.000 live births. Today, there are increasing publications stating that risk factors in the aetiology of CP can be traced back to pre-conception period. However, when risk factors considered, prenatal factors appear as the main cause with a weighted rate of 75%. As our knowledge on etiology mounted up, studies on prevention procedures also accelerated. CP is a clinical diagnosis. Therefore, being alert for risk factors is the first and most important step. CP treatment is planned with an integrative approach together with rehabilitation exercises, medical and surgical treatments. The main goal of programs are to enable children to reach their maximum capacity. Despite the technological advances in medical diagnosis and treatment protocols, CP remains to be the most common cause of paediatric disability in childhood. Considering aspects like risk factors, aetiology, prevention measures, diagnosis and management; there are many questions that need answers.

Keywords: Cerebral palsy, diagnosis, management, risk factors, botulinum toxin A, rehabilitation


Cerebral palsy (CP), is not a defined, separate disease classification, but an umbrella term. The term was first described in 1861 by the English orthopedist William Little. Little has correlated a difficult labour and neonatal hypoxia with limb spasticity and consequential musculoskeletal deformities (1). Although it was first described as a sequela of difficult postpartum hypoxia, we now know that this observation explains a very limited group. CP, which has been expressed in different forms for many years, has been defined in 2006 by an international consensus as “a group of permanent disorders of the development of movement and posture, causing activity limitation that are attributed to non-progressive disturbances that occurred in the developing or fetal brain” (2).

Today, CP still remains as the most common cause of childhood disability with a prevalence of 1.7-3.1 per 1.000 live births. The figure decreases as the development level of the country increases (3,4).

Etiology and Risk Factors

For more than 100 years, the main etiology of CP was believed to be prolonged labour. The outcome was tried to be explained by relating it to hypoxia during or after birth. However, despite significant improvements in medical facilities, birth comfort and postpartum care; over the years the incidence of CP did not decrease as expected (5). Due to this fact, researchers keep conducting epidemiological studies worldwide.

Considering risk factors, it should be kept in mind that not every baby with risk factors results in diagnosis of CP. Data certifies that, approximately 55% of children diagnosed with CP before the age of 1 years did not meet the diagnostic criteria at the age of 7 years (6).

Today, there are increasing publications stating that risk factors in the aetiology of CP can be traced back to pre-conception period. Studies indicate that even maternal sociodemographic characteristics and reproductive history are associated with CP (7,8). However, when risk factors considered, prenatal factors appear as the main cause with a weighted rate of 75%. This figure is followed by risk factors of infantile and neonatal periods with 10% and 18%, respectively (5,9).

Studies have shown that the frequency of defects in brain development are correlated with gestational week. Gestational week (<32 weeks) and birth weight (<2.500 g) and incidence of damage are inversely related to each other (10,11,12).


As our knowledge on etiology mounted up, studies on prevention procedures also accelerated.

Therapeutic hypothermia: Therapeutic hypothermia applications within 6 hours of birth is aimed to prevent ischemic damage by inhibition of inflammatory cascades and apoptotic cellular processes. It has been estimated that 1 out of 8 new-borns to whom this method is applied is prevented from developing CP symptoms (13,14).

Caffeine: Caffeine is also an agent in trial as a prevention measure. Caffeine for apnea of prematurity trial results indicates caffeine reduces the incidence of CP in very low-birth-weight infants (13,15).

Corticosteroids: When steroid administrations are considered adverse data due to administration time is available. Literature dictates warnings for the use of steroids for the prenatal and postnatal period. While the prenatal betamethasone administration in preterm infants is found to reduce the PVL, early (<8 days) postnatal steroid administration is associated with an increase in CP numbers, despite the pulmonary benefits. In 2010, the American Academy of Paediatrics made recommendations to limit the use of postnatal corticosteroids (13,16,17,18).

Magnesium: Administration of magnesium sulfate during the antenatal period is important for neuroprotection in preterm infants. Magnesium sulfate reduces inflammatory effects through pro-inflammatory cytokine suppression. However, the results are varying for obese mothers. It is wise to state that there is no consensus on the results of the application (13,19).

Clinical Features

CP is a clinical diagnosis. Being alert for risk factors is the first and most important step. Early diagnosis and planning treatment without losing time are of vital importance for these children, to reach the highest physical and cognitive level they can be. The correlation between Paediatricians and Physical Medicine and Rehabilitation (PMR) professionals is one of the most important components of this process. Directing risky babies to PMR specialists as soon as possible will prevent delays in diagnosis and treatment plan (20,21).

The compatibility of motor development with chronological age, persistent primitive reflexes and delay in voluntary motor control are important in terms of diagnosis in infants with prenatal, perinatal and postnatal risk factors. However, considering that spasticity is not fully established before 6 months, athetoid movements are not evident until the age of two, and persistent Babinsky reflexes are not significant, it is difficult to make a definitive diagnosis before the age of two (22,23,24). Therefore, every suspected baby should be included in a rehabilitation program without losing time. MRI and laboratory tests to support the neurological evaluation will accelerate the diagnosis process. As in every other subject, differential diagnosis is also crucial in this aspect. It is possible to reach the final result after excluding progressive neurological diseases, metabolic and genetic disorders. Based on the information above The European Database Group (SCPE) has accepted the optimal age as 5 to confirm the diagnosis (25).

Classification: Clinically, CP can be classified by different methods. According to the extremity involvement, the terms hemiplegia, diplegia, tetraplegia is used; According to the dominant tone disorder, it can be defined as spastic, dyskinetic and ataxic. Balf and Ingram (26), Hagberg et al. (27) and SCPE (2006) (25) classifications are available as facilitating tools (Table 1). When predominant symptoms are considered, spastic CP is the most common type of CP with a rate of 70-80%. It is presented with increased deep tendon reflexes, pathological Babinsky response and upper motor neuron syndrome symptoms. When ambulant patients are considered scissoring gait and toe walking are common clinical features due to internally rotated and adducted hips and gastrocnemius spasticity. Dyskinetic or athetoid CP (10-20%) which characterized by abnormally slow, writhing movements of the hands, feet, arms or legs that are exacerbated during periods of stress absent during sleep. The rarest type is ataxic CP (5-10%) which impairs balance and coordination. Wide base gait at ambulation and intentional tremors are presented as main characteristics. In the case of mixed symptoms, SCPE suggestions is that the classification should be done on the basis of the predominant symptoms (9,25,28).

Co-morbidities: Different co-morbidities accompanying motor deficits can be seen in children with a diagnosis of CP. Epilepsy (15-90%), mental retardation (40-65%), speech problems (50%), urinary incontinence (30%), malnutrition and growth retardation (27%), and drooling (10%) are the most common symptoms. To achieve desired goals, rehabilitation plans should be done with co-morbidities taken in consideration (6,28,29,30,31,32,33,34,35).


Non-surgical methods: The aim in the rehabilitation of CP is to provide the child with the optimum function that he/she can perform with his/her existing neuromotor capacity and to either reduce existing complications or prevent possible complications. Therefore, each rehabilitation plan is an individually tailored program for each patient.

Rehabilitation is based on term ‘‘neuroplasticity’’. A term that is used to explain the ability of the nervous system to undergo permanent structural and functional changes in reaction to internal and external stimuli. It works in the case of both a damaged and undamaged brain, which “learns anew” as the result of rehabilitation. The greatest possibilities of modification occur at the earliest stages of development of the central nervous system. It is at this stage that the brain demonstrates a high degree of plasticity, which favours the compensation of various deficiencies. Since the neuroplasticity potential is higher in the early stages of life, it is important to start the treatment of children with CP in the earliest possible period (20,21).

CP management is an integrative approach together with rehabilitation applications, physical therapy modalities, medical and surgical treatments. The main goal in management is to control spasticity, avoid involuntary movements, preserve range of motion, increase function, and enable children to reach their maximum capacity that we can integrate into social life (36).

In rehabilitation programs, neuro-rehabilitative treatment approaches (Bobath, Vojta) form the basis of treatment. Supporting rehabilitation exercises with other modalities such as occupational therapy and speech therapy, and integrating professionals such as psychologists and social workers to the program positively effects the quality and outcome of the treatment. Optimal outcomes require a team approach.

Although it is predicted that intensive treatment programs will lead to more satisfactory results, there is no consensus on the threshold for intensity and duration of rehabilitation programs (37). Analysing rehabilitation programs; it will be noticed that there is no consensus on content, outcomes or long-term gains (38,39,40,41,42,43,44). The reason for the lack of consensus on the results may be attributed to complex clinical feature of the diagnosis and individually tailored nature of the treatment programs. This significant cause result in difficulty in randomization and obtaining the outcomes as numerical data.

Modalities as bracing, kinesiotape, biofeedback and neuromuscular electrical stimulation (NMES) are integral parts of the rehabilitation program.

Bracing: Orthoses prescribed mainly for two different purposes; to prevent deformities and to increase function (45).

Kinesiotape: Kinesiotape was introduced in 1996 by Kenzo Kase to control pain, regulate muscle tone, increase muscle strength, and regulate blood and lymph flow. They are used to increase muscle strength, posture control and spasticity control in the treatment of CP (46).

Biofeedback: Biofeedback application is used to train a single muscle activity in static positions in patients without cooperation deficit. The clinical application of biofeedback to improve a patient’s motor control begins by re-educating that muscle by providing visual or audio feedback of electromyogram, positional or force parameters in real time (47,48).

NMES: NMES is an adjuvant treatment for muscle strengthening and spasticity control, which has been shown to improve motor function in CP treatment programs. Similar to rehabilitation programs, there is no consensus on the intensity, duration and contribution of NMES to treatment outcomes (49).

Botulinum toxin: Botulinum toxin type-A (BoNT-A) is a dose-dependent and reversible agent that blocks presynaptic acetylcholine release at the neuromuscular junction. With the increase in clinical experience in recent years, the agent has become the most widely used medical intervention in children with CP. The evidence is that with the appropriate use of BoNT-A in younger children the onset of fixed equinus might be delayed to a small but important degree, permitting later utilization of orthopaedic surgery at optimum age. This means reduction in the serial operations that children used to be exposed between the ages of 2-8 and ‘‘birthday syndrome’’ has become an out of date term. However, the optimism regarding the prevention of contractures generated by the spastic mouse study has never been translated to the clinical practice and almost all of the children still need release surgery. In the case of in non-ambulatory children Botulinum toxin administration is recommended only for pain relief. The agent has the power of increasing the quality of life with the right patient selection. However, there is still no consensus among practitioners on issues such as treatment protocols and application frequency (50,51,52,53,54,55,56,57,58).

Surgical Interventions

Selective dorsal rhizotomy (SDR): SDR is a surgical method that is performed by the incision of the posterior nerve roots. Surgery is applied for spasticity management. The most appropriate age range for CP patients has been determined as 4-6 years. Although undesirable results such as post-operative deep sensory loss, urinary retention, hypotonia and persistent low back pain have been reported, it is an effective surgical method with satisfactory results with the right case selection in lower extremity spasticity (59).

Orthopaedic surgical interventions: Orthopaedic surgical interventions (release surgery, osteotomy, tendon transferring techniques) which are widely performed in the treatment of CP, are applied with the aim of preventing deformities and correcting the existing deformity. For surgical interventions, it would be appropriate to wait until the age of 6 when the child’s gait pattern matures. The important aspect to keep in mind is the principle of “performing simultaneous multi-level release surgery in one session”. It has been reported that the morbidity of a single session surgical approach is lower compared to multisession surgical approach. When this principle is applied, it has been observed that the results of post-op rehabilitation outcomes are more satisfactory, and the gains at postural and functional improvements are longer lasting (6,36,60,61).


Despite the technological advances in medical diagnosis and treatment protocols, CP remains to be the most common cause of paediatric disability in childhood. Considering aspects like risk factors, etiology, prevention measures, diagnosis and management; there are many questions that need answers.


Peer-review: Externally peer-reviewed.

Financial Disclosure: The author declared that this study received no financial support.


  1. Little WJ. The classic: Hospital for the cure of deformities: course of lectures on the deformities of the human frame. 1843. Clin Orthop Relat Res. 2012;470:1252-1256.
  2. Rosenbaum P, Paneth N, Leviton A, Goldstein M, Bax M, Damiano D, et al. A report: the definition and classification of cerebral palsy April 2006. Dev Med Child Neurol Suppl. 2007;109:8-14.
  3. Sellier E, Platt MJ, Andersen GL, Krageloh-Mann I, De La Cruz J, Cans C, et al. Decreasing prevalence in cerebral palsy: a multi-site European population-based study, 1980 to 2003. Dev Med Child Neurol. 2016;58:85-92.
  4. Yeargin-Allsopp M, Van Naarden Braun K, Doernberg NS, Benedict RE, Kirby RS, Durkin MS. Prevalence of cerebral palsy in 8-year-old children in three areas of the United States in 2002: a multisite collaboration. Pediatrics 2008;121:547-554.
  5. Reddihough DS, Collins KJ. The epidemiology and causes of cerebral palsy. Aust J Physiother. 2003;49:7-12.
  6. Ozel S. Serebral Palsi. In: Beyazova M, Kutsal YG editors. Fiziksel Tıp ve Rehabilitasyon. Istanbul: Gunes Tip Kitapevi; 2011:2681-2724.
  7. Jacobsson B, Hagberg G. Antenatal risk factors for cerebral palsy. Best Pract Res Clin Obstet Gynaecol. 2004;18:425-436.
  8. Durkin MS, Maenner MJ, Benedict RE, Van Naarden Braun K, Christensen D, Kirby RS, et al. The role of socio-economic status and perinatal factors in racial disparities in the risk of cerebral palsy. Dev Med Child Neurol. 2015;57:835-843.
  9. Krigger KW. Cerebral palsy: an overview. Am Fam Physician. 2006;73:91-100.
  10. Prevalence and characteristics of children with cerebral palsy in Europe. Dev Med Child Neurol 2002;44:633-640.
  11. Platt MJ, Cans C, Johnson A, Surman G, Topp M, Torrioli MG, et al. Trends in cerebral palsy among infants of very low birthweight (<1500 g) or born prematurely (<32 weeks) in 16 European centres: a database study. Lancet. 2007;369:43-50.
  12. Himpens E, Van den Broeck C, Oostra A, Calders P, Vanhaesebrouck P. Prevalence, type, distribution, and severity of cerebral palsy in relation to gestational age: a meta-analytic review. Dev Med Child Neurol. 2008;50:334-40.
  13. Shepherd E, Salam RA, Middleton P, Han S, Makrides M, McIntyre S, et al. Neonatal interventions for preventing cerebral palsy: an overview of Cochrane Systematic Reviews. Cochrane Database Syst Rev. 2018;6:CD012409.
  14. Jacobs S, Hunt R, Tarnow-Mordi W, Inder T, Davis P. Cooling for newborns with hypoxic ischaemic encephalopathy. Cochrane Database Syst Rev. 2013;CD003311.
  15. Schmidt B, Roberts RS, Davis P, Doyle LW, Barrington KJ, Ohlsson A, et al. Long-term effects of caffeine therapy for apnea of prematurity. N Engl J Med. 2007;357:1893-1902.
  16. Jacobsson B, Hagberg G, Hagberg B, Ladfors L, Niklasson A, Hagberg H. Cerebral palsy in preterm infants: a population-based case-control study of antenatal and intrapartal risk factors. Acta Paediatr. 2002;91:946-951.
  17. O’Shea TM, Kothadia JM, Klinepeter KL, Goldstein DJ, Jackson BG, Weaver RG, et al. Randomized placebo-controlled trial of a 42-day tapering course of dexamethasone to reduce the duration of ventilator dependency in very low birth weight infants: outcome of study participants at 1-year adjusted age. Pediatrics. 1999;104:15-21.
  18. Watterberg KL, American Academy of Pediatrics. Committee on Fetus and Newborn. Policy statement--postnatal corticosteroids to prevent or treat bronchopulmonary dysplasia. Pediatrics. 2010;126:800-808.
  19. Chollat C, Marret S. Magnesium sulfate and fetal neuroprotection: overview of clinical evidence. Neural Regen Res. 2018;13:2044-2049.
  20. Granild-Jensen JB, Rackauskaite G, Flachs EM, Uldall P. Predictors for early diagnosis of cerebral palsy from national registry data. Dev Med Child Neurol. 2015;57:931-935.
  21. Novak I, Morgan C, Adde L, Blackman J, Boyd RN, Brunstrom-Hernandez J, et al. Early, Accurate Diagnosis and Early Intervention in Cerebral Palsy: Advances in Diagnosis and Treatment. JAMA Pediatr. 2017;171:897-907.
  22. Pellegrino L. Making the diagnosis of Cerebral Palsy. In: Dormans J, Pellegrino L editors. Caring for Children with Cerebral Palsy. Baltimore, USA: Paul H. Brookes Publishing Co.; 1998:31-5.
  23. Apak S, Korkmazlar U. Gelisimsel tani testleri. In: Apak S editors. Gelisim Norolojisi. Istanbul, Turkey: Bayrak Matbaacilik; 1999:219-65.
  24. Matthews D. Cerebral Palsy. In: Molnar G, Alexander M editors. Pediatric Rehabilitation. Philadelphia, USA: Hanley&Belfus; 1999:193-2017.
  25. Christine C, Dolk H, Platt MJ, Colver A, Prasauskiene A, Krageloh-Mann I, et al. Recommendations from the SCPE collaborative group for defining and classifying cerebral palsy. Dev Med Child Neurol Suppl. 2007;109:35-38.
  26. Balf CL, Ingram TT. Problems in the classification of cerebral palsy in childhood. Br Med J. 1955;2:163-166.
  27. Hagberg G, Hagberg B, Olow I. The changing panorama of cerebral palsy in Sweden 1954-1970. III. The importance of foetal deprivation of supply. Acta Paediatr Scand. 1976;65:403-408.
  28. Sucuoglu H. Demographic and Clinical Characteristics of Patients with Cerebral Palsy. Istanbul Med J. 2018;19:219-224.
  29. Leach EL, Shevell M, Bowden K, Stockler-Ipsiroglu S, van Karnebeek CD. Treatable inborn errors of metabolism presenting as cerebral palsy mimics: systematic literature review. Orphanet J Rare Dis. 2014;9:197.
  30. Sigurdardottir S, Eiriksdottir A, Gunnarsdottir E, Meintema M, Arnadottir U, Vik T. Cognitive profile in young Icelandic children with cerebral palsy. Dev Med Child Neurol. 2008;50:357-362.
  31. Darling-White M, Sakash A, Hustad KC. Characteristics of Speech Rate in Children With Cerebral Palsy: A Longitudinal Study. J Speech Lang Hear Res. 2018;61:2502-2515.
  32. Kwong KL, Wong SN, So KT. Epilepsy in children with cerebral palsy. Pediatr Neurol. 1998;19:31-36.
  33. Gururaj AK, Sztriha L, Bener A, Dawodu A, Eapen V. Epilepsy in children with cerebral palsy. Seizure. 2003;12:110-114.
  34. Kulak W, Sobaniec W. Risk factors and prognosis of epilepsy in children with cerebral palsy in north-eastern Poland. Brain Dev. 2003;25:499-506.
  35. Mert GG, Incecik F, Altunbasak S, Herguner O, Mert MK, Kiris N, et al. Factors affecting epilepsy development and epilepsy prognosis in cerebral palsy. Pediatr Neurol. 2011;45:89-94.
  36. Berker N, Yalcin S. The HELP Guide to Cerebral Palsy; 2005.
  37. Hsu CW, Kang YN, Tseng SH. Effects of Therapeutic Exercise Intensity on Cerebral Palsy Outcomes: A Systematic Review With Meta-Regression of Randomized Clinical Trials. Front Neurol. 2019;10:657.
  38. Graham HK, Aoki KR, Autti-Ramo I, Boyd RN, Delgado MR, Gaebler-Spira DJ, et al. Recommendations for the use of botulinum toxin type A in the management of cerebral palsy. Gait Posture. 2000;11:67-79.
  39. Bower E, Michell D, Burnett M, Campbell MJ, McLellan DL. Randomized controlled trial of physiotherapy in 56 children with cerebral palsy followed for 18 months. Dev Med Child Neurol. 2001;43:4-15.
  40. Butler C, Darrah J. Effects of neurodevelopmental treatment (NDT) for cerebral palsy: an AACPDM evidence report. Dev Med Child Neurol. 2001;43:778-790.
  41. Palmer FB, Shapiro BK, Wachtel RC, Allen MC, Hiller JE, Harryman SE, et al. The effects of physical therapy on cerebral palsy. A controlled trial in infants with spastic diplegia. N Engl J Med. 1988;318:803-808.
  42. Damiano DL, Dodd K, Taylor NF. Should we be testing and training muscle strength in cerebral palsy? Dev Med Child Neurol. 2002;44:68-72.
  43. Bobath B. The treatment of neuromuscular disorders by improving patterns of co-ordination. Physiotherapy. 1969;55:18-22.
  44. Knox V, Evans AL. Evaluation of the functional effects of a course of Bobath therapy in children with cerebral palsy: a preliminary study. Dev Med Child Neurol. 2002;44:447-460.
  45. Aboutorabi A, Arazpour M, Ahmadi Bani M, Saeedi H, Head JS. Efficacy of ankle foot orthoses types on walking in children with cerebral palsy: A systematic review. Ann Phys Rehabil Med. 2017;60:393-402.
  46. Karabay İ, Doğan A, Ekiz T, Köseoğlu BF, Ersöz M. Training postural control and sitting in children with cerebral palsy: Kinesio taping vs. neuromuscular electrical stimulation. Complement Ther Clin Pract. 2016;24:67-72.
  47. Fernando CK, Basmajian JV. Biofeedback in physical medicine and rehabilitation. Biofeedback Self Regul. 1978;3:435-455.
  48. Wolf SL. Electromyographic biofeedback applications to stroke patients. A critical review. Phys Ther. 1983;63:1448-1459.
  49. Salazar AP, Pagnussat AS, Pereira GA, Scopel G, Lukrafka JL. Neuromuscular electrical stimulation to improve gross motor function in children with cerebral palsy: a meta-analysis. Braz J Phys Ther. 2019;23:378-386.
  50. Montal M. Botulinum neurotoxin: a marvel of protein design. Annu Rev Biochem. 2010;79:591-617.
  51. Cocco A, Albanese A. Recent developments in clinical trials of botulinum neurotoxins. Toxicon. 2018;147:77-83.
  52. Simpson DM, Gracies JM, Graham HK, Miyasaki JM, Naumann M, Russman B, et al. Assessment: Botulinum neurotoxin for the treatment of spasticity (an evidence-based review): report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology. 2008;70:1691-1698.
  53. Graham HK, Rosenbaum P, Paneth N, Dan B, Lin JP, Damiano DL, et al. Cerebral palsy. Nat Rev Dis Primers. 2016;2:15082.
  54. Hastings-Ison T, Sangeux M, Thomason P, Rawicki B, Fahey M, Graham HK. Onabotulinum toxin-A (Botox) for spastic equinus in cerebral palsy: a prospective kinematic study. J Child Orthop. 2018;12:390-397.
  55. Cosgrove AP, Graham HK. Botulinum toxin A prevents the development of contractures in the hereditary spastic mouse. Dev Med Child Neurol. 1994;36:379-385.
  56. Multani I, Manji J, Hastings-Ison T, Khot A, Graham K. Botulinum Toxin in the Management of Children with Cerebral Palsy. Paediatr Drugs. 2019;21:261-281.
  57. Lundy CT, Doherty GM, Fairhurst CB. Botulinum toxin type A injections can be an effective treatment for pain in children with hip spasms and cerebral palsy. Dev Med Child Neurol. 2009;51:705-710.
  58. Ostojic K, Paget SP, Morrow AM. Management of pain in children and adolescents with cerebral palsy: a systematic review. Dev Med Child Neurol. 2019;61:315-321.
  59. Abbott R. The selective dorsal rhizotomy technique for spasticity in 2020: a review. Childs Nerv Syst. 2020;36:1895-1905.
  60. Nene AV, Evans GA, Patrick JH. Simultaneous multiple operations for spastic diplegia. Outcome and functional assessment of walking in 18 patients. J Bone Joint Surg Br. 1993;75:488-494.
  61. Norlin R, Tkaczuk H. One session surgery on the lower limb in children with cerebral palsy. A five year follow-up. Int Orthop. 1992;16:291-293.