Open access peer-reviewed chapter

Definition, Epidemiology, and Etiological Factors of Cerebral Palsy

Written By

Emine Eda Kurt

Submitted: November 18th, 2015 Reviewed: June 30th, 2016 Published: September 21st, 2016

DOI: 10.5772/64768

Chapter metrics overview

2,148 Chapter Downloads

View Full Metrics


CP is not a diagnosis but an “umbrella term for many clinical descriptions. It refers to a group of permanent disorders of the development of movement and posture, causing activity limitation, that are attributed to nonprogressive disturbances that occurred in the developing fetal or infant brain. The motor disorerders of cerebral palsy are often accompanied by disturbances of sensation, perception, cognition. First description was made in 19th century by William Little. CP prevalence is generally reported around 2-3 per 1000 live births in both developed and developing countries (even if for very different reasons). Additionally for term children CP prevalence is 1 per 1000 live births. This rates are 6-10 times higher in preterm birth. The etiology of CP has been reported very diverse and multifactorial as prenatal, perinatal and postnatal. The causes and risk factors are congenital, genetic, inflammatory, infectious, anoxic, traumatic and metabolic. Knowledge of the epidemiology and etiology of cerebral palsy is important. Thus, at least in some cases, early diagnosis and prevention can be achieved.


  • Cerebral Palsy
  • Definition
  • Epidemiology
  • Etiology
  • Risk factors

1. Definition

Cerebral palsy (CP) is a well-recognized neurodevelopmental condition beginning in early childhood and persisting throughout the lifetime. It was first reported by William little, who was an orthopedic surgeon, in 1843 as cerebral paresis [1, 2]. Little focused on joint contractures and deformities resulting from long-standing spasticity and paralysis. Additionally, he indicated that the cause of the spasticity and paralysis was often due to damage to the brain during infancy and, specifically, preterm birth and perinatal asphyxia [3].

The most comprehensive study until then was published in 1862 by William Little. The association between a large number of patients’ clinical presentation and their birth history as recalled by the family was described in this study. Little differentiated between the congenital deformities observed at the time of birth, such as talipes equinovarus, and the limb deformities that developed subsequently to preterm, difficult, or traumatic births, which he termed as spastic rigidity. It was described as a disorder that appeared to strike children in the first year of life, affected developmental skill progression, and did not improve over time [4].

Then, Sarah McNutt described that it continued to raise the profile of the risks of long-term disability arising from birth trauma [5]. At the end of the nineteenth century, Sigmund Freud suggested that CP might be rooted in the brain’s development in the womb and related aberrant development to factors influencing the developing fetus [2, 6, 7]. In addition, in the early 1920s, some 30 years after Freud’s comments, an American orthopedic surgeon made the next major contribution for understanding of CP [8].

In the twentieth century, newer documented concepts of cerebral palsy have been defined. Mac Keith and Polani [1, 8] described CP as “a persisting but not unchanging disorder of movement and posture, occurring in the early years of life due to a nonprogressive disorder of the brain, the result of interference during its development.” In 1964, Bax [9] reported a description of CP suggested by an international working group that has become a classic and is still used. It was expressed that CP is a disorder of movement and posture due to a defect or lesion of the immature brain. Although this definition is usually all that is cited by authors, some additional comments were added by Bax: “For practical purposes it is usual to exclude from cerebral palsy those disorders of posture and movement which are of short duration, due to progressive disease or due solely to mental deficiency.” Bax and his group felt that this simple sentence can be readily translated into other languages and hoped that it may be used universally. At that time, it was felt wiser not to define completely what they meant by immature brain, as any such description may be restricted services to those in need. Like its predecessors, this formulation of the CP concept placed an exclusive focus on motor aspects and also stressed the specific consequences of early as opposed to late-acquired brain damage. It was not formally included in the concept that cognitive, sensory, behavioral, and other associated impairments were very prevalent in people with disordered movement and posture due to a defect or lesion of the immature brain, a frequent significant disability. This definition continued to emphasize the motor impairment and acknowledged its variability, previously underscored in the MacKeith and Polani definition; it also excluded progressive disease, a point introduced in Bax’s annotation [8]. The heterogeneity of disorders covered by the term of CP, as well as advances in understanding of development in infants with early brain damage, led Mutch et al. [10] to modify the definition of CP in 1992 as follows: an umbrella term covering a group of nonprogressive, but often changing, motor impairment syndromes secondary to lesions or anomalies of the brain arising in the early stages of development.

To underline the idea that a comprehensive approach to CP needs to be multidimensional and that management of patients with CP almost always requires a multidisciplinary setting, classes of disorders commonly accompanying CP have been identified and included in the revised definition [1]. And last definition of CP, which is comprised to prior assessments and identifications, was made in April 2006. CP describes a group of persistent disorders of the development of movement and posture causing activity limitations that are attributed to nonprogressive disturbances that occurred in the developing fetal or infant brain. The motor disorders of cerebral palsy are often accompanied by disturbances of sensation, perception, cognition, communication, and behavior by epilepsy and secondary musculoskeletal problems. This description was authored by the members of the executive committee functioning in panels enriched with expertise from consultants and by comments and suggestions from many reviewers responding to drafts provided to the international community. It is offered for international consensus and adoption, with the intent of providing a broad spectrum of audiences with a common conceptualization about cerebral palsy [1]. CP is defined as a group of nonprogressive, but often changing, motor impairment syndromes secondary to lesions or abnormalities of the brain and emerging in the early stages of development [10]. CP is a symptom complex rather than a disease. It is a concept derived from an insult to a growing, developing brain and therefore it is a dynamic changing clinical picture emanating from static pathology [11]. CP may be diagnosed during the first two years of life, especially when functional impairment is mild [12, 13].

This specification contains the concept that CP is a group of neurodevelopmental disorders that involve numerous developing functions. As in other neurodevelopmental disorders, various manifestations of the disordered brain may appear more significantly in different persons or at different life periods, e.g., some aspects of the motor impairment, sensory loss, attentional difficulty, epilepsy, musculoskeletal dysfunction, intellectual disability, and many others maybe more prominent or more problematic at different periods of the life of a person with CP [1].

In 2010, Blair again emphasized that CP is not a diagnosis but an “umbrella term for many clinical descriptions.” It has covered a wide variety of clinical conditions that meet the following four criteria:

  1. - The presence of a disorder of movement or posture.

  2. - Secondary to a cerebral abnormality.

  3. - Arising early in development.

  4. - By the time movement impairment exists, the cerebral abnormality is static.

There is no test, genetic, metabolic, immunologic, or otherwise, that demonstrates the existence or absence of CP because there is no specified cause, cerebral pathology, or even type of motor impairment resulting from nonprogressive cerebral pathology acquired early in life. Even as a clinical description, these criteria fail in several aspects to achieve the precision required of a definition [14, 15]. For example, specifying the age at which development is no longer considered “early.” There is no agreement on this age [16].

Because it is difficult to definitively differentiate between pre- and neonatally acquired brain damage, all those not postneonatally acquired are usually considered together. The four criteria cannot be addressed until (a) motor development can be clearly recognized as being normal or disordered and (b) the possibility of progressive cerebral disease can be excluded. Signs suggesting disordered motor control may be recognized very early in life, but accurate prediction has only been confirmed by trained observers in the small proportion of persons with CP born very preterm [17]. Acquisition of the cerebral abnormality may precede recognition of the motor disorder by many months or even years. However, brain-impaired infants, particularly the most severely impaired, are at increased risk of dying before reaching an age at which the criteria for CP can be confirmed. Early death is a competing outcome. On the other hand, it is difficult to definitively exclude the possibility of progression or resolution at any age. Even if cerebral pathology is static, motor abilities change in all children over time, even if that development is grossly abnormal, making functional change an unreliable marker for progressive cerebral pathology. Conversely, a proportion of children described as CP at an early age catch up with their normally developing peers at a later age [18]. Therefore, the choice of an age that must be attained before being counted as CP, as well as the age beyond which development is no longer early, is arbitrary and depends on the interest in using the CP label. Treating clinicians are more flexible in applying the CP label because their primary concern is to balance the psychological effects of labeling a child having CP with the therapeutic opportunities that the label can afford. This balance can change with time. Registers with a long lifespan require primarily a constant definition over time, and this was the guiding principle of the recommendation by Badawi et al. [19] that conditions historically excluded from CP (not “diagnosed” as CP on account of having another diagnosis) continue to be excluded, even if meeting the criteria for CP. By contrast, reliability between current observers is the guiding principle of the more recent multicenter surveillance system in Europe, which adopted a flowchart to decision inclusion or exclusion of cases of cerebral palsy on registration [20]. However, the reality of barriers to achieving interobserver agreement of classification is demonstrated by the relatively poor agreement achieved with this flowchart [21]. Diagnosis of CP is not easy. It needs time to be confirmed. Premature diagnosis leading to over-ascertainment (because of transient anomalies in preterm babies) or under-ascertainment, as stated above, is not an unchanging condition with the clinical aspect in some cases altering as a child develops. There is consensus that 5 years of age was the optimal age for confirmation of diagnosis [22].


2. Epidemiology

CP prevalence is usually reported around 2–3 per 1000 live births in both developed and developing countries for very different reasons [23, 24]. For term children, CP prevalence is 1 per 1000 live births. Additionally, for moderately preterm children (32–36 weeks’ gestation), forecasts are 6–10 times higher and for very preterm children (less than 32 weeks’ gestation), prevalence is 10 times higher than the moderately preterm children. CP rates for live births show a lower prevalence for babies of birthweight less than 1000 g than for those with a birthweight of 1000–1499 g. This paradoxical effect is caused from the high number of babies who do not live long enough to develop CP and it disappears when forecasting prevalence for neonatal survivors. Changes in perinatal and neonatal mortality accelerated in most countries from the 1960s, with a huge decrease up until the late 1980s, when there was an increase in the absolute number of children with CP. From 1990s, there has been a plateauing of mortality rates but a downward trend in CP rates, mainly in moderate and very low birthweight (VLBW) children. In most studies, the CP rates in children born at term or with normal birthweight seem rather stable over time. This finding is especially relevant since normal birthweight and term children represent at least one-half of children with CP and, thus, it may be connected to the persisting stagnation of CP prevalence, despite continuous improvement in perinatal care and in mortality rates [2527].

There were different rates of CP reported in recent five decades from different population. Published rates from geographically defined populations show significant differences, primarily due to variations in methods (Table 1). Variations within a reporting system over time tend to be smaller [28].

The proportion of children described as CP increases with decreasing gestational age at birth. The advent of mechanical ventilation to neonatal intensive care has allowed survival of increasingly preterm births, creating a new source of high-risk neonates and perhaps a new cause of brain damage [27].

AreaYear rangeNumber of casesRate of per 1000
Turkey [2931]1990–2006
Sweden [32]1995–19981701.9
Canada [33]1991–19952.7
U.S.A. [34]20024163.6
Australia [35]1970–1998
United Kingdom [36]1984–2002
Norway [37]1996–19983742.1
Danimark [38]1971–1974
France [39]1980–19892611.78

Table 1.

Published rates of CP from population-based samples.


3. Etiological factors

The etiology of CP is very diverse and multifactorial. The causes are congenital, genetic, inflammatory, infectious, anoxic, traumatic, and metabolic. The injury to the developing brain may be prenatal, natal, or postnatal [40]. Due to the lack of a definitive test for CP, multiple and different possible causes also constitute a challenge in this context. For more than 30% of children, there are no risk factors or known etiology [41, 42] but some risk factors have repeatedly been observed to be related to CP [43]. CP may result from one or more etiologies and can occur at any stage from before conception to infancy, with the actual cause difficult to determine in all cases [41, 42, 44]. Known causes according to the timing of the brain insult can be classified, respectively, as prenatal, perinatal, and postnatal.

3.1. Prenatal causes of cerebral palsy

Among the important known causes of cerebral palsy are congenital brain malformations including malformations of cortical development. Modern imaging techniques enable more children with these conditions to be identified [45, 46]. Currently, problems occurring during intrauterine development, congenital disorders, asphyxia occurring in any gestational age, and preterm birth are thought to account for the majority of cases [47]. Neuroimaging studies support the current thought that prenatal causes of CP, such as brain malformations, intrauterine vascular malformations, and infection, are more common than birth asphyxia [48]. Although intrapartum asphyxia was originally thought to be a major reason for CP, it accounts for only 10–20% of cases. The most frequent perinatal or neonatal etiologies in low birthweight infants are periventricular leukomalacia (PVL), periventricular hemorrhage, and cerebral infarction, but in infants of normal birthweight, the most common reason is hypoxicischemic encephalopathy. Knowledge about the cortical dysplasias, of which some have a genetic basis, is increasing rapidly [49]. Periventricular leukomalacia is a risk factor with 60–100% of patients with PVL developing CP. In general, congenital malformations are strongly associated with cerebral palsy [5054]. Other known antenatal causes of cerebral palsy are vascular events demonstrated by brain imaging (for example, middle cerebral artery occlusion), and maternal TORCH (toxoplasmosis, rubella, cytomegalovirus, and herpes simplex) infections during the first and second trimesters of pregnancy are the known causes of long-term neurodevelopmental disabilities. In industrialized countries, the proportion of CP attributable to TORCH infections is estimated to be almost 5% [13]. The less common causes of cerebral palsy include metabolic disorders, maternal ingestion of toxins, and rare genetic syndromes [55].

3.2. Perinatal causes

Antepartum hemorrhage, obstructed labor, or cord prolapse can jeopardize the fetus causing hypoxia, but essential criteria must be fulfilled before cerebral palsy can be attributed to the acute intrapartum period [56, 57]. These criteria are metabolic acidosis in umbilical arterial cord, fetal scalp or very early neonatal blood samples, and early onset of severe or moderate neonatal encephalopathy in infants of >34 weeks gestation [57].

Children with cerebral palsy, who have a history of neonatal encephalopathy, are more likely to have had signs of intrapartum hypoxia such as meconium staining of the amniotic fluid [58]. However, there may be no evidence of perinatal asphyxia in a significant percentage of children with neonatal encephalopathy [19]. In a systematic study, cerebral palsy was more strongly associated with encephalopathy [59]. Severe hypoglycaemia, untreated jaundice, and severe neonatal infection in neonatal period may be responsible for cerebral palsy [55].

3.3. Postnatal causes

Infection and injuries are responsible for most cases of postneonatally acquired cerebral palsy in developed countries. Thanks to introduction of new vaccines, meningitis and subsequent neurological sequelae were decreased in a large number of children. Accidental (motor vehicle accidents and near-drowning episodes) and nonaccidental injuries may responsible for cerebral palsy. Other reasons of postneonatally acquired cerebral palsy contain apparent life-threatening events, cerebrovascular accidents, and following surgery for congenital malformations. Meningitis, septicemia, malaria, and other conditions are the important causes of cerebral palsy in developing countries [55].

The risk factors associated with CP may also be presented as maternal, paternal and sibling factors, prenatal factors, perinatal factors, and postnatal factors.

3.4. Maternal, paternal, and sibling factors

Maternal medical conditions are associated with cerebral palsy. These include intellectual disability, seizures [60], maternal thrombophilia [33], and thyroid disease [50, 60]; prior reproductive loss [61] and CP in a sibling have been reported as an association with CP in the Collaborative Perinatal Project of the National Institute of Neurological and Communicative Disorders and Stroke [60]. Adolescent pregnants are likely to have low gestational weeks, low birthweight, and birth traumas. Maternal age > 35 years was reported among risk factors of CP [13]. Öztürk et al. [30] also reported that mothers of children with CP were significantly younger, with an increase in adolescent pregnancies. Mothers of children with CP had low gestational weeks, low birthweight, and prolonged labor.

Parental consanguinity [62, 63] and low economic status were found related to CP in two studies [64, 65].

3.5. Prenatal risk factors

Preeclampsia is associated with an increased risk of cerebral palsy in term infants [66] but this association does not seem to exist in preterm infants [67, 68]. It has been suggested that preeclampsia may lead to a release of catecholamines in preterm infants, which accelerates fetal maturation [69], but care is needed in comparing rates in infants of the same gestation, given that preeclampsia itself can be directly responsible for preterm births. Alternatively, the presence of preeclampsia may result in elective preterm delivery, avoiding the inflammatory responses of spontaneous preterm labors with all their associated problems.

Chorioamnionitis and intrauterine infection and/or inflammation are well-known risk factors for CP. Prenatal maternal chorioamnionitis is accounting for as much as 12% of cerebral palsy in term infants and 28% in premature infants [13, 70, 71]. According to the inflammatory hypothesis, maternal infection can lead to elevated fetal blood and brain cytokine levels, which might result in central nervous damage and subsequent CP [13]. Nelson et al. reported that blood inflammatory cytokine levels in term infants that developed CP were significantly higher than control groups [72]. A number of studies have shown that even fever itself might be harmful. There may be toxic products of the infecting organisms or toxic effects of inflammatory mediators produced by the mother, infant, or placenta. It is tempting to consider that cytokines or other inflammatory mediators induced brain damage directly or indirectly [73, 74]. Gilles et al. [75] demonstrated that maternal trauma in pregnancy may be implicated as a possible cause of cerebral palsy. Antepartum hemorrhage is also associated with mortality, CP, and white matter damage in preterm infants [76].

Multiple pregnancies, also reported as a risk factor of CP, increase fourfold in twins and 18-fold in triplets [77]. These are associated with preterm delivery, poor intrauterine growth, birth defects, and intrapartum complications [78, 79].

Intrauterine growth restriction (IUGR) can be responsible to increase risk of neonatal morbidity and mortality, and also seems to affect brain development [80]. In some specific variance in the brain of IUGR infants, as restriction of the volume of gray matter, a reduced amount of the total DNA in glia cells and neurons, and changes in cerebral hemodynamic have been reported. This hypothesis supported by animal studies showed reduced oxygen delivery to the brain and retarded growth of the forebrain and cerebellum [81, 82]. Several mechanisms have been suggested for the relation between IUGR in term babies and CP. The abnormal growth may play a direct role in causing CP or utero brain injury. Alternatively, a separate process, such as placental insufficiency, could cause both the growth retardation and brain injury [83, 84].

Two mutations have been detected, which predispose heterozygous carriers to venous thrombosis. One is a mutation localized to the factor V gene (factor V Leiden mutation, VL) and second is the gene for prothrombin [85, 86]. Nelson et al. reported that placental thrombosis, or neonatal stroke, may have occurred and resulted in CP [72].

Males are at higher risk of CP, perhaps because of the recently identified gender-specific neuronal vulnerabilities [15, 87]. In the fetus, CP has been associated with intrauterine growth restriction [88, 89] maternal factors [90, 91], other risk factors [92], and congenital anomalies not only of the brain, head, eyes, and face, but also with noncerebral anomalies (in the apparent absence of cerebral anomalies), particularly of the heart, limbs, and skeleton [93, 94]. The risk of CP also increases with the number of suboptimal factors affecting a pregnancy [50, 95].

3.6. Perinatal risk factors

According to the results of World Health Report, perinatal asphyxia and high-risk pregnancy were independent factors that correlated with CP in term and near-term newborns. In developing countries, 4–9 million infants experience birth asphyxia annually [96]. Major events likely to cause perinatal asphyxia include prolonged delivery, breech delivery, and emergency cesarean births [54, 97]. Though intrapartum factors producing asphyxia were traditionally accepted to be the principal cause of CP, this assumption was reconsidered during the 1980s and 1990s, and today it is suggested that 70–80% of cases of CP are due to prenatal factors and that birth asphyxia plays a relatively minor role. Although intrapartum asphyxia is believed to account for around 10% of CP in term and near-term infants, Swedish population-based CP report by the Hagberg group detected birth asphyxia to be the likely cause of CP in 28% of term children with CP [98]. However, “birth asphyxia” is a poorly defined term related to a sequence initiated by hypoxia and its clinical signs are nonspecific [43]. Using indirect signs of birth asphyxia, recent studies suggest that birth asphyxia might not be such an important cause of CP as was previously assumed, but that it might sometimes constitute one element of a multifactorial cause; neonatal signs associated with birth asphyxia might be early manifestations of CP from a variety of causes, of which birth asphyxia is only one; and the majority of pathways to CP commence antenatally [13, 43, 99]. Any factor causing a very preterm birth that lies on a potential causal path to CP must be remembered. Many etiologic studies control or stratify the risk of CP that also increases with the number of suboptimal factors affecting a pregnancy [100].

The lower birthweights and shorter gestations associated with multiple birth contribute significantly to their higher risk of CP, but cannot be the only relevant factors because gestation-specific rates are higher for multiples than for singletons born at term or extremely preterm [101, 102]. The most important risk factor seems to be prematurity, and low birthweight with risk of CP increasing with decreasing gestational age and birthweight. About 28% of CP cases are born very preterm, compared to 1% of all births. As an effect of the success of neonatal intensive care during the last three decades, ensuring an increasing survival of children born extremely preterm, the prevalence of CP among preterm children has risen [103]. These groups of children may contribute significantly to the overall number of children with CP since they are at greater risk of developing CP. Although it can be expected that where mortality rates are high and CP rates are low, It may be that thanks to good clinical practice and developing technology mortality and CP prevalence rate will be reduced. Neonatal intensive care practices, including withdrawal of life support, may have an impact on local CP rates over time; this influence is difficult to assess [13, 104].

Abruptio placentae have also been suggested to be associated with a higher risk of CP, especially moderately preterm (32–36 weeks) groups [105]. Perinatal infections (bacterial, viral, and protozoal) may also cause the development of CP [106].

Other relations with cerebral palsy include prolonged rupture of the membranes in infants of all gestations [52] and in preterm babies [67]; the presence of meconium-stained fluid [107] and tight nuchal cord was also reported as associated with CP [108].

3.7. Postnatal risk factors of CP

Postneonatally acquired CP is said to result from a recognized brain damaging event that is unrelated to factors in the antenatal or perinatal period, but there is a growing realization that the pathway to postneonatally acquired CP often begins before the postneonatal period [19]. The inclusion criteria for a postneonatal time range of the insult vary between reports. Some researchers have included cases acquired from neonatal causes that might have had their origin during pregnancy, labor, or delivery [109]. Although a strict definition of beyond 28 days is used by others [16], the upper age limit also varied from 2 to 10 years between researchers [110]. Population-based estimates of the frequency of postneonatally acquired CP, as a proportion of all CP, are reported in the literature to change between 1.4 and 24%, with higher rates in undeveloped and developing countries, and lower socio-economic groups [16]. The Surveillance of Cerebral Palsy in Europe, in a cohort of children from eight countries born between 1976 and 1990, reported that the rate of children whose CP was of postneonatal origin was 7.8% [39]. Pharoah et al. suggested that postnatal causes are generally resulted in spastic CP [111]. Most surveillance systems distinguish cases in which motor impairment is obviously acquired postneonatally, usually following cerebral infection or head trauma [16]. Other infection complications, cerebrovascular accidents, trauma, hypoxia, gastroenteritis, and other causes of acute encephalopathy, neoplasmas, and exposure toxins were other reasons that are reported [112]. Infection, however, remains an important cause of acquired CP despite a fall in the overall numbers more than 30 years of the study. With the introduction of new vaccines, the proportion of cases due to infection will be further decrease, providing there is adequate education and regular control [16].

CP is a nonprogressive but permanent disorder. The disease has been better understood by the researchers in due course of time, and then described as “CP is not a diagnosis but an umbrella term.” Though there are different rates according to the region, percentage of CP is not low in especially developing and undeveloped countries. Etiological factors of CP are very diverse and may be classified according to time period (prenatal, perinatal, postneonatal) and parenteral factors. It may be that, thanks to good clinical practice and developing technology, the prevalence of CP rate will be reduced and additionally most known risk factors will be avoided.


  1. 1. Rosenbaum P, Paneth N, Leviton A, Goldstein M, Bax M, et al. A report: the definition and classification of cerebral palsy April 2006. Dev Med Child Neurol Suppl 2007;109:8–14.
  2. 2. Morris C. Definition and classification of cerebral palsy: a historical perspective. Dev Med Child Neurol 2007;49(109):3–7.
  3. 3. Little WJ. Lectures on the deformity of the human frame. Lancet 1843;1:318–320.
  4. 4. Little WJ. On the incidence of abnormal parturition, difficult labour, premature birth and asphyxia neonatorurn on the mental and physical condition of the child, especially in relation to deformities. Trans Obstetr Soc London 1862;3:293–344.
  5. 5. McNutt SJ. Apoplexia neonatorum. Am J Obstetr 1885;1:73.
  6. 6. Freud S. Les diplegies cerebrales infantiles. Rev Neurol 1893;1:177–183.
  7. 7. Accardo PJ. Freud on diplegia: commentary and translation. Am J Dis Child 1982;136:452–456.
  8. 8. Mac Keith RC, Polani PE. The little club: memorandum on terminology and classification of cerebral palsy. Cerebral Palsy Bull 1959;5:27–35.
  9. 9. Bax MCO. Terminology and classification of cerebral palsy. Dev Med Child Neurol 1964;l6:295–307.
  10. 10. Mutch LW, Alberman E, Hagberg B, Kodama K, Velickovic MV. Cerebral palsy epidemiology: where are we now and where are we going? Dev Med Child Neurol 1992;34:547–555.
  11. 11. Brown K. Cerebral palsy: can we prevent it? Dev Med Child Neurol Suppl 2003;95:30.
  12. 12. Ford GW, Kitchen WH, Doyle LW, et al. Changing diagnosis of cerebral palsy in very low birthweight children. Am J Perinatol 1990;7(2):178–181.
  13. 13. Jacobsson B, Hagberg G. Antenatal risk factors for cerebral palsy. Best Pract Res Clin Obstet Gynaecol 2004;18(3):425–436.
  14. 14. Blair E, Love S. Commentary on the definition and classification of cerebral palsy. Dev Med Child Neurol 2005;47:510.
  15. 15. Stanley F, Blair E, Alberman E. ‘What are the cerebral palsies?’ Cerebral Palsies: Epidemiology and Causal Pathways. London: MacKeith Press; 2000;pp. 8–13, Chapter 2.
  16. 16. Reid S, Lanigan A, Reddihough D. Post-neonatally acquired cerebral palsy in Victoria, Australia, 1970–1999. J Paediatr Child Health 2006;42(10):606–611.
  17. 17. Constantinou J, Adamson-Macedo E, Mirmiran M, et al. Movement, imaging and neurobehavioural assessment as predictors of cerebral palsy in preterm infants. J Perinatol 2007;27(4):225–229.
  18. 18. Nelson KB, Ellenberg JH. Children who ‘outgrew’ cerebral palsy. Pediatrics 1982;69(5):529–536.
  19. 19. Badawi N, Watson L, Petterson B, et al. What constitutes cerebral palsy? Dev Med Child Neurol 1998;40:520–527.
  20. 20. Surveillance of Cerebral Palsy in Europe (SCPE) Surveillance of cerebral palsy in Europe: a collaboration of cerebral palsy surveys and registers. Dev Med Child Neurol. 2000;42(12):816–824.
  21. 21. Gainsborough M, Surman G, Maestri G, Colver A, Cans C. Validity and reliability of the guidelines of the surveillance of cerebral palsy in Europe for the classification of cerebral palsy. Dev Med Child Neurol 2008;50(11):828–831.
  22. 22. Cans C, Dolk H, Platt MJ, et al. Recommendations from the SCPE collaborative group for defining and classifying cerebral palsy. Dev Med Child Neurol 2007;49(109):35–38.
  23. 23. Nelson KB. Can we prevent cerebral palsy? N Engl J Med 2003;349:1765–1769.
  24. 24. Kadhim H, Sébire G, Kahn A, Evrard P, Dan B. Causal mechanisms underlying periventricular leukomalacia and cerebral palsy. Curr Pediatr Rev 2005;1:1–6.
  25. 25. Tu J, Willison D, Silver F, et al. Impracticality of informed consent in the registry of the Canadian Stroke Network. N Engl J Med 2004;350:1414–1421.
  26. 26. Ingelfinger J, Drazen J. Registry research and medical privacy. N Engl J Med 2004;350(14):1452.
  27. 27. Aly H. Mechanical ventilation and cerebral palsy. Pediatrics 2005;115(6):1765–1766.
  28. 28. Blair E. Epidemiology of the cerebral palsies. Orthopedic Clinics of North America 2010;41(4):441-455.
  29. 29. Serdaroglu A, Cansu A, Özkan S, Tezcan S. Prevalence of cerebral palsy in Turkish children between the ages of 2 and 16 years. Dev Med Child Neurol 2006;48(6):413–416.
  30. 30. Öztürk A, Demirci F, Yavuz T, et al. Antenatal and delivery risk factors and prevalence of cerebral palsy in Duzce (Turkey). Brain Dev 2007;29(1):39–42.
  31. 31. Okan N, Okan M, Eralp O, Aytekin AH. The prevalence of neurological disorders among children in Gemlik (Turkey). Dev Med Child Neurol 1995;37(7):597–603.
  32. 32. Himmelmann K, Hagberg G, Beckung E, et al. The changing panorama of cerebral palsy in Sweden. IX. Prevalence and origin in the birth-year period 1995–1998. Acta Paediatr 2005;94:287–294.
  33. 33. Smith L, Kelly K, Prkachin G, et al. The prevalence of cerebral palsy in British Columbia, 1991–1995. Can J Neurol Sci 2008;35(3):342–347.
  34. 34. Yeargin-Allsopp M, Van Naarden Braun K, Doernberg N, et al. Prevalence of cerebral palsy in 8-year-old children in three areas of the United States in 2002: a multisite collaboration. Pediatrics 2008;121(3):547–554.
  35. 35. Reid SM, Lanigan A, Walstab JE, et al. The Victorian Cerebral Palsy Register. Melbourne, Australia: Murdoch Childrens’ Research Institute; 2005.
  36. 36. Surman G, Newdick H, King A, Gallagher M, Kurinczuk JJ. Child: four counties database of cerebral palsy, vision loss, and hearing loss in children. Annual report 2008: including data for births 1984 to 2002. Oxford, UK: National Perinatal Epidemiology Unit; 2008.
  37. 37. Andersen G, Irgens L, Haagaas I, et al. Cerebral palsy in Norway: prevalence, subtypes and severity. Eur J Paediatr Neurol 2008;12(1):4–13.
  38. 38. Uldall P, Michelsen SI, Topp M, Madsen M. The Danish cerebral palsy registry. Dan Med Bull 2001;48: 161–163.
  39. 39. Surveillance of cerebral palsy in Europe (SCPE). Prevalence and characteristics of children with cerebral palsy in Europe. Dev Med Child Neurol 2002;44(9):633–640.
  40. 40. Sankar C, Mundkur N. Cerebral palsy—definition, classification, etiology and early diagnosis. Indian J Pediatr 2005;72(10):865–868.
  41. 41. Taft LT. Accentuating the positive for children with cerebral palsy. Except Parent 1999;29:64–66.
  42. 42. Rosembaum P. Cerebral palsy: what parents and doctors want to know. Brit Med J 2003;326:970–974.
  43. 43. Blair E, Stanley F. Issues in the classification and epidemiology of cerebral palsy. Mental Retard Dev Disabil Res Rev 2002;3:184–193.
  44. 44. Jones MW, Morgan E, Shelton CE, Thorogood C. Cerebral palsy: introduction and diagnosis (Part I). J Pediatr Health Care 2007;21:146–152.
  45. 45. Krageloh-Mann I, Petersen D, Hagberg G, Vollmer B, Hagberg B, Michaelis R. Bilateral spastic cerebral palsy—MRI pathology and origin: analysis from a representative series of 56 cases. Dev Med Child Neurol 1995;37:379–397.
  46. 46. Steinlin M, Good M, Martin E, Banziger O, Largo RH, Boltshauser E. Congenital hemiplegia: morphology of cerebral lesions and pathogenetic aspects from MRI. Neuropediatrics 1993;24:224–229.
  47. 47. Moster D, Lie R, Irgens L, Bjerkedal T, Markestad T. The association of Apgar score with subsequent death and cerebral palsy: a population-based study in term infants. J Pediatr 2001;138:798–803.
  48. 48. Truwit CL, Barkovich AJ, Koch TK, Ferriero DM. Cerebral palsy: MR findings in 40 patients. Am J Neuroradiol 1992;13:67–78.
  49. 49. Dobyns WB, Truwit CL. Lissencephaly and other malformations of cortical development: 1995 update. Neuropediatrics 1995;26:132–147.
  50. 50. Blair E, Stanley F. Etiological pathways to spastic cerebral palsy. Paediatr Perinatal Epidemiol 1993;7:302–317.
  51. 51. Croen L, Grether J, Curry C, Nelson K. Congenital abnormalities among children with cerebral palsy: more evidence for prenatal antecedents. J Pediatr 2001;138:804–812.
  52. 52. Nelson KB, Ellenberg JH. Predictors of low and very low birth-weight and the relation of these to cerebral palsy. JAMA 1985;254:1473–1479.
  53. 53. Palmer L, Blair E, Petterson B, Burton P. Antenatal antecedents of moderate and severe cerebral palsy. Paediatr Perinatal Epidemiol 1995;9:171–184.
  54. 54. Torfs CP, van den Berg BJ, Oechsil FW, Cummins S. Prenatal and perinatal factors in the etiology of cerebral palsy. J Pediatr 1990;116:615–619.
  55. 55. Reddihough DS, Collins KJ. The epidemiology and causes of cerebral palsy. Aust J Physiother 2003;49(1):7–12.
  56. 56. Muraskas J, Ellsworth L, Culp E, Garbe G, Morrison J. Risk management in obstetrics and neonatal-perinatal medicine. In: Özdemir Ö (Ed). Complementary Pediatrics 2012, pp. 269–286. InTech, Available from: pediatrics/common allegations-of-professional-liability-against-practitioners-of-neonatal-perinatal-medicine; DOI: 10.5772/32846
  57. 57. MacLennan A. For the international cerebral palsy task force: a template for defining a causal relation between acute intrapartum events and cerebral palsy: international consensus statement. BMJ 1999;319:1054–1059.
  58. 58. Gaffney G, Flavell V, Johnston A, Squier M, Sellars S. Cerebral palsy and neonatal encephalopathy. Arch Dis Child 1994;70:195–200.
  59. 59. Van de Riet JE, Vandenbussche FP, Le Cessie S, Keirse MJ. Newborn assessment and long-term adverse outcome: a systematic review. Am J Obstetr Gynaecol 1999;180:1024–1029.
  60. 60. Nelson KB, Ellenberg JH. Antecedents of cerebral palsy. Multivariate analysis of risk factors. New Engl J Med 1986:315:81–86.
  61. 61. Blair E, Stanley FJ. When can cerebral palsy be prevented? The generation of causal hypotheses by multivariate analysis of a case-control study. Paediatr Perinat Epidemiol 1993;7:272–301.
  62. 62. Sinha G, Corry P, Subesinghe D, et al. Prevalence and type of cerebral palsy in a British ethnic community: the role of consanguinity. Dev Med Child Neurol 1997;39(4):259–262.
  63. 63. Erkin G, Delialioglu S, Ozel S, et al. Risk factors and clinical profiles in Turkish children with cerebral palsy: analysis of 625 cases. Int J Rehabil Res 2008;31(1):89–91.
  64. 64. Dowding VM, Barry C. Cerebral palsy: social class differences in prevalence in relation to birthweight and severity of disability. J Epidemiol Community Health 1990;44:191–195.
  65. 65. Kramer MS, Goulet L, Lydon J, et al. Socio-economic disparities in preterm birth: causal pathways and mechanisms. Pediatr Perinatal Epidemiol 2001;15:104–123.
  66. 66. Collins M, Paneth N. Pre-eclampsia and cerebral palsy: are they related? Dev Med Child Neurol 1988;40:207–211.
  67. 67. Murphy DJ, Sellars S, MacKenzie IZ, Yudkin P, Johnson A. Case-control study of antenatal and intrapartum risk factors for cerebral palsy in very preterm singleton babies. Lancet 1995;346:1449–1454.
  68. 68. Spinillo A, Capuzzo E, Cavallini A, Stronati M, De Santolo A, Fazzi E. Preeclampsia, preterm delivery and infant cerebral palsy. Eur J Obstetr Gynecol Reprod Biol 1998;7:151–155.
  69. 69. Amiel-Tison C, Pettigrew C. Adaptive changes in the developing brain during intrauterine stress. Brain Dev 1991;13:67–76.
  70. 70. Grether JK, Nelson KB, Walsh E, et al. Intrauterine exposure to infection and risk of cerebral palsy in very preterm infants. Arch Pediatr Adolescent Med 2003;157(1):26–32.
  71. 71. Iliodromiti Z, Zygouris D, Karagianni P, et al. Brain injury in preterm infants. In: Raines D (Ed.). Neonatal Care 2012, pp. 73–86. Rijeka: InTech, Available from; DOI: 10.5772/52078
  72. 72. Nelson KB, Dambrosia JM, Grether JK, Phillips TM. Neonatal cytokines and coagulation factors in children with cerebral palsy. Ann Neurol 1998;44(4):665–675.
  73. 73. Nelson KB, Willoughby RE. Infection, inflammation and the risk of cerebral palsy. Curr Opin Neurol 2000;13(2):133–139.
  74. 74. Nelson KB, Grether JK, Dambrosia JM, Dickens B, Phillips TM. Cytokine concentrations in neonatal blood of preterm children with cerebral palsy. Am J Obstet Gynecol 2000;182:47.
  75. 75. Gilles MT, Blair E, Watson L, et al. Trauma in pregnancy and cerebral palsy: is there a link? MJA 1996;164:500–501.
  76. 76. Stanley FJ, Blair E, Alberman E. Cerebral palsies: epidemiology and causal pathways. Clinics in Developmental Medicine. London: MacKeith Press; 2000. p. 151.
  77. 77. Stanley F, Blair E, Alberman E. ‘The special case of multiple pregnancy’. Cerebral Palsies: Epidemiology and Causal Pathways. London: MacKeith Press; 2000. pp. 109–124, Chapter 10.
  78. 78. Livinec F, Ancel PY, Marret S, et al. The risk of mortality or cerebral palsy in twins: a collaborative population-based study. Pediatr Res 2002;52:671–681.
  79. 79. Little S, Ratcliffe J, Caughey A. Cost of transferring one through five embryos per in vitro fertilization cycle from various payor perspectives. Obstet Gynecol 2006;108(3):593–601.
  80. 80. Clausson B, Gardosi J, Francis A, Cnattingius S. Perinatal outcome in SGA births defined by customized versus population-based birthweight standards. BJOG 2001;108(8):830–834.
  81. 81. Jensen A, Klonne HJ, Detmer A, Carter AM. Catecholamine and serotonin concentrations in fetal guinea-pig brain: relation to regional cerebral blood flow and oxygen delivery in the growth-restricted fetus. Reprod Fertil Dev 1996;8(3):355–364.
  82. 82. Rees S, Mallard C, Breen S, et al. Fetal brain injury following prolonged hypoxemia and placental insufficiency: a review. Compar Biochem Physiol A. Mol Integr Physiol 1998;119(3):653–660.
  83. 83. Scherjon SA, Oosting H, Smolders-DeHaas H, et al. Neurodevelopmental outcome at three years of age after fetal ‘brain-sparing’. Early Hum Dev 1998; 52(1):67–79.
  84. 84. Uvebrant P, Hagberg G. Intrauterine growth in children with cerebral palsy. Acta Paediatr 1992;81(5):407–412.
  85. 85. Ridker PM, Miletich JP, Hennekens C, Buring JE. Ethnic distribution of factor V Leiden in 4047 men and women, implications for venous thromboembolism screening. JAMA 1997;277:1305–1307.
  86. 86. Thorarensen O, Ryan S, Hunter J, Younkin DP. Factor V Leiden mutation: an unrecognized cause of hemiplegic cerebral palsy, neonatal stroke and placental thrombosis. Ann Neurol 1997;42:372–375.
  87. 87. Johnston M, Hagberg H. Sex and the pathogenesis of cerebral palsy. Dev Med Child Neurol 2007;49(1):74–78.
  88. 88. Jacobsson B, Ahlin K, Francis A, et al. Cerebral palsy and restricted growth status at birth: population-based case-control study. BJOG 2008;115(10):1250–1255.
  89. 89. Glinianaia S, Jarvis S, Topp M, et al. Intrauterine growth and cerebral palsy in twins: a European multicenter study. Twin Res Hum Genet 2006;9(3):460–466.
  90. 90. Nelson K. Thrombophilias, perinatal stroke, and cerebral palsy. Clin Obstet Gynecol 2006;49(4):875–884.
  91. 91. Gibson C, MacLennan A, Hague W, et al. Associations between inherited thrombophilias, gestational age, and cerebral palsy. Am J Obstet Gynecol 2005;193(4):1437.
  92. 92. Hong T, Paneth N. Maternal and infant thyroid disorders and cerebral palsy. Semin Perinatol 2008;32(6):438–445.
  93. 93. Garne E, Dolk H, Krageloh-Mann I, et al. Cerebral palsy and congenital malformations. Eur J Paediatr Neurol 2008;12:82–88.
  94. 94. Blair E, Al Asedy F, Badawi N, et al. Is cerebral palsy associated with birth defects other than cerebral defects? Dev Med Child Neurol 2007;49(4):252–258.
  95. 95. Nelson KB. Causative factors in cerebral palsy. Clin Obstet Gynecol 2008;51(4):749–762.
  96. 96. World Health Organization: World Health Report 1998: Life in the twenty first century: a vision for all. Geneva. World Health Organization; 1998.
  97. 97. Powell TG, Pharoah POD, Cooke RWI, Rosenbloom L. Cerebral palsy in low-birthweight infants. I. Spastic hemiplegia: associations with intrapartum stress. Dev Med Child Neurol 1988;30:11–18.
  98. 98. Hagberg B, Hagberg G, Beckung E, Uvebrant P. Changing panorama of cerebral palsy in Sweden. VIII. Prevalence and origin in the birth year period 1991–94. Acta Paediatr 2001;90(3):271–277.
  99. 99. Blair E, Stanley FJ. Intrapartum asphyxia: a rare cause of cerebral palsy. J Pediatr 1988;112(4):515–519.
  100. 100. Blair E, deGroot J. Prediction or causation: the nature of the association between maternal pre-eclampsia and cerebral palsy. Dev Med Child Neurol 2008;50:32.
  101. 101. Scher A, Petterson B, Blair E, et al. The risk of mortality or cerebral palsy in twins: a collaborative population-based study. Pediatr Res 2002;52:671–681.
  102. 102. Muraskas J, DeGregoris L, Rusciolelli C, Sajous C. Preterm birth of extremely low birth weight infants. In: Morrison J (Ed). Preterm Birth-Mother and Child 2012, pp. 263–274. Rijeka: InTech Open Access Publisher. Available from: infants; DOI: 10.5772/32802.
  103. 103. Littenberg B, MacLean C. Passive consent for clinical research in the age of HIPAA. J Gen Intern Med 2006;21(3):207–211.
  104. 104. Cans C, De-la-Cruz J, Mermet MA. Epidemiology of cerebral palsy. Paediatr Child Health 2008;18(9):393–398.
  105. 105. Jacobsson B, Hagberg G, Hagberg B, et al. Cerebral palsy in preterm infants: a population-based casecontrol study of antenatal and intrapartal risk factors. Acta Paediatr 2002;91(8):946–951.
  106. 106. Sanchez PJ. Perinatal infections and brain injury: current treatment options. Clin Perinatol 2002; 29(4):799–826.
  107. 107. Walstab J, Bell R, Reddihough D, Brennecke S, Bessell C, Beischer N. Antenatal and intrapartum antecedents of cerebral palsy a case-control study. Aust NZ J Obstetr Gynaecol 2002;42:138–146.
  108. 108. Nelson KB, Grether JK. Potentially asphyxiating conditions and spastic cerebral palsy in infants of normal birth weight. Am J Obstetr Gynecol 1998;179:507–513.
  109. 109. Laisram N, Srivastava VK, Srivastava RK. Cerebral palsy—an etiological study. Indian J Pediatr 1992; 59:723–728.
  110. 110. Stanley F, Blair E, Alberman E. Post neonatally acquired cerebral palsy: incidence and antecedents. Cerebral Palsies: Epidemiology and Causal Pathways. London: MacKeith Press; 2000. pp. 124–137, Chapter 11.
  111. 111. Pharoah P, Cooke T, Rosenbloom L. Acquired cerebral palsy. Arch Dis Child. 1989;64:1013–1016.
  112. 112. Kerem Günel M, Türker D, Ozal C, Kaya Kara O. Physical management of children with cerebral palsy. In: Emira Svraka (Ed). Cerebral Palsy-Challenges for the Future 2014. pp. 29–73. Rijeka: Available from:; DOI: 10.5772/57505

Written By

Emine Eda Kurt

Submitted: November 18th, 2015 Reviewed: June 30th, 2016 Published: September 21st, 2016