E-ISSN 1858-8360 | ISSN 0256-4408

Review Article

Online Publishing Date:
08 / 01 / 2024



2023; Vol 23, Issue No. 2


Determinants of cerebral palsy in children: systematic review

Kaleab Tesfaye Tegegne (1)

Department of Public Health, College of Health Science, Debark University, Debark, Ethiopia

Correspondence to:

Kaleab Tesfaye Tegegne

Department of Public Health, College of Health Science, Debark University, Debark, Ethiopia.

Email: kaleabtesfaye35 [at] gmail.com

Received: 09 December, 2022 | Accepted: 26 March 2023

How to cite this article:

Tegegne KT. Determinants of cerebral palsy in children: systematic review. Sudan J Paediatr. 2023;23(2):126–144.



Cerebral palsy (CP) is a group of disorders of movement and postural control caused by a nonprogressive defect or lesion of the developing brain. Several prepregnancy risk factors have been described including maternal age, parity and maternal diseases including epilepsy, diabetes and thyroid disease. There are few in-depth studies on the causes of CP. In the present systematic review, databases searched were Google Scholar and PubMed to identify data on determinants of CP in the world. Studies were included if they specifically mentioned CP as an outcome, the study objective is to identify factors associated with CP in children and all quantitative observational studies. JBI Critical Appraisal Tools were used to assess the methodological quality of a study. Papers that meet the inclusion criteria were rigorously appraised by two critical appraisers. 40 consistent determinants of CP in children from 95 research articles that meet inclusion criteria are included in the review. The majority of studies (24 articles) showed that premature babies and low weight were determinants of CP in children, whereas 15 studies showed that low Apgar scores were determinants of CP in children. The commonest determinants of CP in children are premature babies and low weight, low Apgar scores, intrauterine infection, congenital brain malformations, thyroid disease, premature rupture of membrane (PROM) and placental abruption. Preventing preterm delivery, low birth weight and intrauterine infection as well as immediate neonatal resuscitation for newborns with low Apgar scores may help to prevent CP in children.


Cerebral palsy; Determinants.


Cerebral palsy (CP) is a group of disorders of movement and postural control caused by a nonprogressive defect or lesion of the developing brain [1]. According to population-based research conducted worldwide, the prevalence estimates for CP range from 1.5 to more than 4 per 1,000 live births [26]. In general, there are 2 cases of CP per 1,000 live births [79].

Chronic neurological conditions like CP place a heavy cost on the National Health System since they have a negative psychological and social impact on families. Medical and rehabilitation teams must work together to manage the treatment and rehabilitation of CP [10,11].

Prenatal, perinatal and neonatal risk factors are connected to CP. Perinatal asphyxia only accounts for less than 10% to 20% of instances of CP, with premature birth acknowledged as the primary risk factor [1216]. Prematurity is one of the main CP risk factors [17,18].

Maternal age, parity and maternal illnesses such as epilepsy, diabetes and thyroid disease have all been listed as prepregnancy risk factors [19,20]. Risk factors that appear early or late in pregnancy include assisted reproduction, male gender, congenital malformations, multiple pregnancies and intrauterine growth restriction [21,22].

Fetal distress, premature rupture of the membrane, precipitous labor and jaundice are the key risk factors for CP [23]. In contrast, in a different study, the predictors were male gender, higher birth order, vaginal operations, central nervous system (CNS) illnesses in infants, unknown maternal education status and history of newborn hospital admissions [24].

Instrumental deliveries are risk factors for CP [25] and according to studies from Nigeria [26], Uganda [27] and Botswana [28], CP is linked to a history of CNS illness. Two studies found that CP risk factors were preterm and birth weight less than 1.5 kg [29,30]. Maternal anemia, maternal hypertension, pre-eclampsia, antepartum hemorrhage, eclampsia and multiple pregnancies are antenatal risk factors for CP [31].

Other African research has also implicated postnatal causes such as perinatal hypoxia, bilirubin encephalopathy, intracranial infections, ischemic stroke and congenital brain deformities as causal factors [3234]. A Tanzanian study found that CP is mostly associated with prenatal issues [35]. A Ghanaian study also revealed that the most significant and curable risk factor for the onset of CP was severe neonatal hyperbilirubinemia [36].

Since CP is a chronic condition, it is essential to research and examine its causes, risk factors and interventional treatments to properly understand and manage the condition [37]. There are few in-depth studies on the causes of CP. A thorough discussion of risk factors linked to CP is provided in this systematic review. This systematic review identified CP risk factors that can be avoided, which lowers the prevalence of the condition. In this review, I have so tried to pinpoint the causes of CP in children. For the creation of preventive measures and treatments, a deeper comprehension of the CP etiology is required. The purpose of this review was to determine the factors that influence CP in children around the world. This systematic review identified consistent determinants of CP in children in two or more studies and this will help to develop a standard questionnaire as well as to construct a conceptual framework on determinants of CP in children.


To gather information on the global drivers of CP, I carried out a systematic evaluation of the literature that was available. Any study’s abstract from anywhere in the world was evaluated for inclusion. Criteria for inclusion were when the purpose of the study is to discover factors linked with CP in children, the study addressed CP as an outcome and all quantitative observational studies.

The preferred reporting items for the systematic review and meta-analysis (PRISMA) 2020 checklist were followed (http://www.prisma-statement.org/).

Search strategy

To locate pertinent English-language publications, various search techniques were used. I searched the databases of Google Scholar and PubMed using the terms ‘CP’, ‘determinants’, ‘risk factors’, and ‘CP’. I searched the World Health Organisation and international disability organisations’ websites for additional references that the previous search had overlooked. After screening the abstracts of any papers found using this search approach for relevance, the full texts of all pertinent articles were downloaded. A snowballing search was conducted after references from each pertinent article were checked for other pertinent articles. 95 research publications were included in the final review.

Studies quality assessment tool

JBI Critical Appraisal Tools available from (https://synthesismanual.jbi.global) for analytic crossectional study, case-control study and cohort study depending on study design used by researchers that meet the inclusion criteria were used to assess the methodological quality of a study and to determine the extent to which a study has addressed the possibility of bias in its design, conduct and analysis. All of the items in the checklist are rated based on the author’s subjective judgment given responses to the items rated as yes or no. Two reviewers independently evaluated the articles using the JBI critical appraisal checklist and the PRISMA checklist to determine whether they should be included in the review.

All papers that meet the inclusion criteria were rigorously appraised by two critical appraisers.


95 research publications on determinants of CP in the world meet inclusion criteria and are included in the review [2331,38123]. A summary of CP risk factors in the included studies is presented in Table 1. The risk factors of CP are included in the identified list if the factors are associated with CP in two or more studies. I have identified 40 consistent risk factors of CP in children from 95 research articles that meet inclusion criteria and are included in the review.

Factors seen in three categories:

  1. Prenatal factors: Changes in coagulation, toxemia, untreated maternal hypothyroidism, chorioamnionitis, placental infarction, multiple pregnancies, autoimmune disease, cerebral arterial infarction, high blood pressure, intrauterine infection, trauma, genetic factors and exposure to toxins and drugs.
  2. Perinatal factors: Premature childbirth, prenatal asphyxia, hyperbilirubinemia, prenatal infection, low weight, maternal fever during childbirth, systemic or CNS infection, maintained hypoglycemia and intracranial hemorrhage.
  3. Postnatal factors: Head injuries, meningoencephalitis, intracranial hemorrhage, cerebral infarction, hydrocephalus, intracranial tumor, convulsive status, respiratory cardio attack, poisoning and severe dehydration [29,30,48] (Figure 2).

Prenatal risk factors associated with CP are urinary tract infection at pregnancy, transvaginal bleeding, perinatal hypoxia and prematurely, while postnatal risk factors are jaundice and convulsive syndrome [46]. Figure 1 shows the List of determinants of CP into four categories: Prenatal, perinatal, preconception and neonatal and infant period.

Prematurity, low birth weight, twins or greater multiple births and prenatal infection are the main risk factors for CP (51). There were identified intrapartum-related, neonatal respiratory depression, neonatal encephalopathy and infections among the prenatal and perinatal determinants (neonatal sepsis, pneumonia, CNS infection, such as meningitis and encephalitis). There have been reports of postneonatal causes such as trauma, pneumonia and sepsis. Low socioeconomic status has also been linked to a higher chance of developing CP [49].

Congenital brain abnormalities, particularly defects of cortical development, are the primary causes of CP. More children with these problems can be diagnosed thanks to modern imaging techniques [5658]. CP and congenital abnormalities are closely related [19,38,39,73,74]. In addition, there are more defects outside of the CNS in children with congenital brain deformities [122].

Other recognised prenatal causes of CP include maternal illnesses during the first and second trimesters of pregnancy (rubella, cytomegalovirus and toxoplasmosis) and vascular events seen by brain imaging (middle cerebral artery occlusion). Among the less frequent causes of CP are metabolic conditions, prenatal exposure to chemicals and uncommon genetic diseases. Neonatal encephalopathy is a clinically recognised syndrome that affects the neurological development of the term infant in the first few days of life. It is characterised by difficulties with breathing induction and maintenance, depression of tone and reflexes, subnormal levels of consciousness and frequent seizures [123].

Children with CP who have a history of neonatal encephalopathy are more likely than children without such a history to exhibit intrapartum hypoxia symptoms, such as meconium staining of the amniotic fluid, as well as a more severe form of the condition [68]. Using a grading system of 0 to III, a systematic investigation found a stronger correlation between CP and Sarnat Grade III encephalopathy than Sarnat Grade II encephalopathy [95].

CP may be caused by neonatal issues such as severe hypoglycemia, untreated jaundice and severe neonatal infection. Surgical procedures for congenital abnormalities and cerebrovascular accidents are two causes of postneonatally acquired CP [40].

Risk factors before pregnancy

Long intermenstrual intervals, irregular menstruation and delayed menstruation are all related to an increased incidence of CP in mothers [39]. CP has also been linked to pregnancies that were particularly close together or far apart [39,103]. Low social class and CP are linked in children with normal birth weight, according to two studies [70,71]. In a study of preterm newborns, parity of three or more was a factor [57]. There is a connection between CP and past fetal fatalities, according to several researchers [73,81]. CP is linked to a number of maternal health issues. These include intellectual disability [73], seizures [73] and thyroid disease [19,73].

Figure 1. PRISMA 2020 flow diagram.

Table 1. Summary of risk factors of CP on the included studies (N=95).

Serial number Risk factors of CP Study reference number
1 PROM [23,3845]
2 Jaundice [23,41,46,47]
3 History of CNS infection [23,2630,48,49]
4 Premature babies, low weight [2930,39,40,42,43,46,48,5065]
5 Maternal hypertension [2931,43,48,60]
6 Convulsive status [2930,46,48]
7 Multiple pregnancy [2930,41,48,50,66,67]
8 Neonatal encephalopathy [49,50,51]
9 Low socio-economic status [51,7074]
10 Congenital brain malformations [9,38,39,62,63,7277]
11 Parity [78,79]
12 Delayed onset of menstruation, irregular menstruation, or long intermenstrual intervals [38,39,80]
13 Previous fetal deaths [73,81]
14 Thyroid disease [19,28,29,40,44,48,73,8284]
15 Pre-eclampsia [30,51,59,85,86]
16 Maternal trauma in pregnancy [28,29,48,87]
17 Chorioamnionitis [28,29,47,51,80,88,89,90]
18 Low Apgar scores [42,56,57,6062,64,65,9196]
19 Neonatal seizures [39,42,56,61,81,97]
20 Sepsis [19,98,99]
21 Respiratory disease [42,81]
22 Untreated maternal anemia [30,58]
23 Hyperbilirubinemia [32,42,59,100,101]
24 Advanced paternal age [58,62,102]
25 Diabetes Mellitus [40,44,59,60,83,84]
26 An unusually short or long interval between pregnancies [39,103]
27 Emergency Cesarean section [107,108112,44,113]
28 Instrumental deliveries [60,25,107,108112]
29 Urinary tract infection during pregnancy [47,58]
30 Placental abruption [39,42,104,105109,85]
31 Exposure to methyl mercury during pregnancy [82,111]
32 Familial aggregation of CP (genetics) [73,112114]
33 history of impaired fertility and its treatment [79,104,105109]
34 Threat of abortion [115,116]
35 Spontaneous abortion [42,104,105109]
36 Maternal medications (antibiotics and anti-epileptics) during pregnancy [115,83,84]
37 Intrauterine infection [41,116,104,105109,86,117,118]
38 Antepartum fever [119,120]
39 Hemolytic disease of newborns [116,121]
40 Gender [23,56]

Figure 2. Determinants of cerebral palsy in children [107112].

Paternal and sibling factors

Sibling and paternal factors are rarely mentioned. More people with athetoid/dystonic CP have older fathers [102]. According to the Collaborative Perinatal Project of the National Institute of Neurological and Communicative Disorders and Stroke, motor deficiency in a sibling has been linked to CP [73].


Risk factors during pregnancy

Pregnancy-induced hypertension increases the risk of CP in children [59,79]. Pre-eclampsia is not associated with an increased risk of CP in preterm infants [51,86]. It has been suggested that preeclampsia may lead to a release of catecholamines in preterm infants, which accelerates fetal maturation [124].

Gestational diabetes increases the risk of CP in children [59,60]. Maternal trauma in pregnancy has been implicated as a possible cause of CP [87]. The rate of CP was increased in children whose mothers received thyroid hormone or estrogen in pregnancy [38] and with maternal thyroid abnormalities [19,82].

Two variants have been found that put heterozygous carriers at risk for venous thrombosis. One is the most frequent cause of familial thrombosis and is a mutation that is specific to the Factor V gene (Factor V Leiden mutation, VL). The prothrombin gene is the second. Caucasian women have a carrier frequency of 4.8%, compared to 5.5% in Caucasian men [125]. Current research in this area was sparked by a report of three infants with hemiplegic CP who were heterozygous for the Factor V Leiden mutation [126]. It was hypothesised that neonatal stroke or placental thrombosis may have occurred in the three cases documented and caused hemiplegia.

Inflammatory mediators and indicators of autoimmune and coagulation disorders seem to be linked to CP [127]. Multiple pregnancies are linked to preterm labor, inadequate intrauterine growth, birth abnormalities and intrapartum problems in children [67,42,68]. Multiple pregnancies are also linked to CP in children [41,66,67]. However, the increased risk of prematurity and low birth weight in twins does not fully account for the increased risk of CP [128]. The loss of one twin during a monochorionic twin pregnancy is acknowledged as a significant risk factor for the co-twin who survives developing CP. The neurological growth of the surviving twin may be hampered during gestation if one twin passes away [135].

The main risk factor for the onset of CP appeared to be a lack of appropriate prenatal care. Infections during pregnancy were identified as significant risk factors. [130]. Some risk factors have repeatedly been observed to be related to CP, i.e., intrauterine viral infections (e.g., rubella and cytomegalovirus) [84,120121], iodine deficiency [134], exposure to methyl mercury during pregnancy [82,111] and in Popayán, the main risk factor was maternal urinary tract infection [57]. Moreover, in another study, the most significant risk factors for the formation of CP were: untreated maternal anemia and the age of the mother over 30 years [58]. According to one study, term newborns with any disease during pregnancy, such as maternal hypertension, were more likely to have CP [60].

According to the gestational age group and clinical CP subtype, CP causes can differ to some extent. While spastic diplegia (legs affected more than arms) is the most common form of spastic involvement in preterm and very preterm newborns, hemiparetic (1-sided) and quadriparetic (4-limb) CP are the most common clinical subtypes in term and near-term infants. A perinatal stroke is a cerebrovascular accident that happens 28 days after birth while the baby is still a fetus or a newborn [93]. Compared to childhood or any other phase up to late middle age, the perinatal period has a significantly higher rate of stroke [59].

Newborns who are abnormally little or huge are more likely to get perinatal stroke than babies who are close to the average weight for the given dates [132]. Perinatal stroke has been linked to primiparity and a history of poor fertility and its treatment [78]. Perinatal stroke can cause CP in children.

The risk of CP is higher in twins than in singletons and it is even higher in triplets. According to the available data, twin pregnancies and high-order multiple births’ propensity for early delivery and infant deaths account for the majority of factors that influence the risk of CP in multiple gestations. The highest incidence of CP was found among twins who survived whose co-twin was stillborn (4.5%), died soon after delivery (6.3%), or had CP (11.8%) in research that covered more than a million births [67].

Populations with high rates of consanguinity have documented familial aggregation of CP, and a national Swedish database found that families had an elevated chance of developing CP [112]. Preterm birth, placental abruption, preeclampsia and chorioamnionitis are a few maternal and pregnancy diseases that are risk factors for CP and have a genetic component. Many of the thrombophilias that cause prenatal strokes have hereditary roots. CP risk has been associated with genetic variations of apolipoprotein E [114] and a few inflammatory cytokines [113].

Exploratory research reveals that CP risk is influenced by nitric oxide synthase polymorphisms. [133,134]. The findings of research to date are consistent with roles for inflammation, coagulation, blood flow regulation and vascular endothelium function in the placenta and brain in CP pathobiology.

Long maternal menstrual intervals have been linked to CP risk in three sizable population-based studies [38,39,80]. Polycystic ovarian syndrome (PCOS) is a significant contributor to abnormal menstrual spacing and is linked to other risk factors for CP, including perinatal stroke, obesity, preeclampsia, a procoagulant and proinflammatory state, preterm birth and the need for special care for the newborn [135].

In term newborns, maternal thyroid illness has been linked to CP [38], a decline in IQ [136] and congenital deafness [137]. During the antenatal period, placental abnormalities [138], intrauterine infections (TORCH infections), genital tract infections [116] and the threat of abortion [115,116], are the factors associated with CP in children.

Meta-analysis showed that maternal hypertension during pregnancy was a risk factor for CP in children [43]. Maternal diabetes mellitus (DM) and thyroid diseases were more significant factors for CP in preterm patients [40,44], and in another study same result was found that maternal conditions (DM, thyroid diseases and medications during pregnancy) are risk factors for CP [83,84]. Antenatal determinants of CP are maternal medications (antibiotics and anti-epileptics) during pregnancy [115] and pre-eclampsia, in low–middle-income settings [64,65]. The main prenatal factor associated with CP was advanced mother age [58,62,102].

Risk factors during labor

Prolapsed cord, substantial intrapartum hemorrhage, protracted or violent birth due to cephalopelvic disproportion or atypical presentation, a large infant with shoulder dystocia and maternal shock from a variety of causes are major factors prone to induce perinatal asphyxia. [39]. The longer second stage of labor has also been linked to CP [81], emergency cesarean section [79], premature separation of the placenta [38] and abnormal fetal position [39].

When taking these elements into account, it is crucial to keep in mind that the event itself might not be the causal factor; instead, the event might just be linked to one or more actual causal factors.

Significant evidence has recently emerged that chorioamnionitis, in particular, intrauterine exposure to infection in the final stages of pregnancy and after labor, is a significant risk factor for CP, especially in term newborns [51,80,88,89]. Chorioamnionitis was discovered to be a risk factor for both CP and periventricular leucomalacia in a meta-analysis of studies that examined the relationship between clinical and histological chorioamnionitis and CP or periventricular leukomalacia in both preterm and full-term infants [139]. It is necessary to learn more about how infections affect the prenatal period.

Other associations with CP include prolonged rupture of the membranes in infants of all gestations [38] and preterm babies [51], the presence of meconium-stained fluid [84,90] and tight nuchal cord [127]. It has been suggested that magnesium sulfate, given for severe pre-eclampsia, is a protective factor in the development of CP in preterm infants [140,141].

CP risk increases with decreasing birth weight [39,51,54,55]. Both the gestational age at delivery and intrauterine growth affect birth weight. The length of gestation is the biggest predictor of CP, and the risk of the condition rises with advancing age at delivery [40]. Poor intrauterine growth also increases the risk of CP [94,95], particularly in moderately preterm [40]. It is not a major risk factor in very preterm infants [51,78].

There may be a connection between the rising number of low birth-weight babies with CP and their survival and future brain damage from birth defects such as intraventricular hemorrhage. Alternately, these children may have already been harmed before birth, and their preterm birth may have resulted from the same circumstances that affected them.

Low placental weight [39] and low Apgar scores are strongly associated with CP [95]. Children with scores of 0–3 at five minutes had an 81-fold increased risk of CP [96]. Prematurity, low birth weight and asphyxia were selected risk factors related to the development of CP [56]. Delivery in a nonhospital setting appeared to be the major factor contributing to the development of CP. Important risk factors identified were home delivery and consanguinity [130].

Some risk factors have repeatedly been observed to be related to CP, i.e., low gestational age [52,53], low Apgar scores [94], preterm delivery and asphyxia [57]. Thus, the most significant risk factors for the formation of CP were tight entanglement of the umbilical cord and fetal hypoxia [58].

Maternal risk factors for CP include maternal infection, placental insufficiency and instrumental delivery. Perinatal factors include low birth weight [59]. One study showed that perinatal asphyxia, childbirth weight and delayed crying were independent factors associated with CP in term newborns [60]. Causal factors for spastic diplegia include evidence of intrauterine infection and PROM [41].

In a population-based study in northern California, evidence of maternal infection or fever during the admission for delivery was associated with the risk of CP in infants of normal birth weight, and with admission to a neonatal intensive care unit, neonatal seizures and meconium aspiration [120]. Chorioamnionitis and perhaps other infections seem to be a common antecedent to encephalopathy in the neonate and to later CP [145]. Repeated observations documented that intrauterine exposure to indicators of inflammation is linked with CP risk and that this is a common cause of low Apgar scores, other signs of neonatal depression, and CP risk [143].

Spontaneous abortion, abruptio placenta, prelabour rupture of membranes and prematurity were associated with a higher risk of CP. Preterm labor, Cesarean section, prematurity, asphyxia and low birth weight (<2500 g) were associated with an increased risk of CP [42]. During the intranatal period, uterine rupture increases the risk of CP in children [138].

The perinatal risk factors such as preterm, low birth weight and birth asphyxia, had a significant association with the development of CP [61]. Early membrane rupture, early delivery and emergency cesarean sections were all linked to an increased risk of CP in infants, according to a meta-analysis [43]. In preterm patients, persistent membrane rupture and maternal hemorrhage were the more important risk factors for CP [40,44]. Another study also found an association between CP and emergency CS [110].

Determinants of CP are PROM of long duration [45], antepartum fever [119], vaginal bleeding [85] and low birthweight (LBW) in low–middle-income settings [64,67]. Perinatal asphyxia was implicated as a cause of CP [64,65,91,92]. The main perinatal factors associated with CP were low Apgar scores, low birth weight and reduced gestational age [62].

Risk factors in the newborn period

Neonatal seizures [39,81], sepsis [19] and respiratory disease are associated with CP [81]. Reported risk factors in the preterm infant include patent ductus arteriosus, hypotension, blood transfusion, prolonged ventilation, pneumothorax, sepsis, hyponatremia, total parenteral nutrition, seizures and parenchymal damage with appreciable ventricular dilatation detected by cerebral ultrasound [97]. Neonatal seizures, in particular, are strongly associated with the risk of CP [39,97]. Gender and epilepsy were selected risk factors related to the development of CP [57].

Respiratory distress syndrome, prolonged ventilation, septicemia, meningitis, hyperbilirubinemia, neonatal seizures and severe cranial ultrasound abnormality were associated with an increased risk of CP in the neonatal period. In the postnatal period, the influence of indirect bilirubin on subcortical structures [116,121,144], hemolytic disease of newborns [121,144], septic conditions [98] and neonatal seizures had a significant association with the development of CP [61].

It is considered that the presence and severity of hypoxic-ischemic encephalopathy during the neonatal period is the strongest predictor of CP [32]. Kernicterus continues to be a significant problem in developing countries despite progress in the management of hyperbilirubinemia. In a clinic-based review in Nigeria, it was found that hyperbilirubinemia was the most common cause of CP [32]. This result is similar to another study [101]. Sepsis has been proven to increase the risk of developing CP, especially in preterm [99]. The antenatal risk factor of CP is CNS malformation [85].

In settings with few resources, there is a higher risk of newborn encephalopathy, according to studies from Nepal and Zimbabwe [47,146]; this may in turn increase the risk of developing CP.

Increased levels of kernicterus been seen in research from West Africa [100] and outcome studies in Zimbabwe have revealed that 20% of newborns with severe jaundice dev have elop CP or motor impairment later in life [47]. The higher rates of jaundice reported are probably caused by untreated neonatal sepsis, G6PD deficiency, ABO and rhesus incompatibility, as well as by the delayed diagnosis and treatment of jaundice [147]. Malformation and small for gestational age births are still strongly linked to CP in children delivered moderately or late preterm [63].

Role of brain imaging

Evidence on the timing of bad occurrences can be obtained via brain imaging, particularly magnetic resonance imaging (MRI). For instance, periventricular leukomalacia develops between the 28th and 34th week of pregnancy, and term infants with perinatal asphyxia have cortical and subcortical gliosis and atrophy in the parasagittal watershed areas. Cortical dysplasias also begin early in pregnancy, between the 12th and 20th week [148]. Despite being a major predictor of CP in preterm infants, periventricular leukomalacia is frequently seen in term infants, indicating that the detrimental event happened long before birth. Periventricular leukomalacia-causing factors may shed light on CP’s potential causes. [90,149]. According to studies, CP is linked to even the mother’s sociodemographic traits and reproductive history [150,151].

Prevention of CP

Within six hours of birth, therapeutic hypothermia is applied to prevent ischemia damage by stifling inflammatory cascades and apoptotic cellular processes. According to estimates, this treatment prevents the onset of CP symptoms in 1 in 8 newborns who receive it [152,153].

A substance being tested as a preventative measure is caffeine. The results of the caffeine for apnea of prematurity experiment show that caffeine lowers the incidence of CP in newborns with very low birth weight [152,154].

Early (8 days) postnatal steroid therapy is related to an increase in CP numbers despite the pulmonary advantages of prenatal betamethasone administration in preterm infants. The year 2010 saw recommendations from the American Academy of Pediatrics to reduce the use of postnatal corticosteroids [150,152,155,156].

Preterm newborns’ neuroprotection depends on the prenatal administration of magnesium sulfate. Through the reduction of pro-inflammatory cytokines, magnesium sulfate lowers the effects of inflammation. For mothers who are obese, the outcomes differ. It is prudent to note that there is disagreement on the application’s outcomes [152,157].

Infants with prenatal, perinatal and postnatal risk factors should have their motor development matched to their chronological age, with any residual primitive reflexes and delays in voluntary motor control being key diagnostic indicators. However, it is challenging to make a conclusive diagnosis before the age of two given that spasticity is not fully developed before 6 months, athetoid movements are not noticeable until the age of two, and persistent Babinsky reflexes are not noteworthy [158160].

Therefore, without delay, every suspected baby should be enrolled in a rehabilitation program. The neurological examination will be supported by an MRI and laboratory testing, which will hasten the diagnosing procedure. Differential diagnosis is essential in this area as it is in every other area. After metabolic, hereditary and progressive neurological diseases have been ruled out, the conclusion is still possible. The European Database Group (SCPE) has determined that five is the ideal age to confirm a diagnosis based on the information above [161].

Further research into the involvement of infection in the prenatal period, studies into the impact of coagulation and inflammatory variables, and the use of advanced brain imaging are anticipated to yield more knowledge regarding the causes of CP. Current studies on the factors contributing to CP will be a crucial starting point for creating prevention methods. I would like to advocate addressing CP’s preventable causes, as doing so can lead to improved practice.


The commonest determinants of CP in children are premature babies and low weight, low Apgar scores, intrauterine infection, congenital brain malformations, premature rupture of the membranes and placental abruption.

Preventing preterm delivery, low birth weight and intrauterine infection as well as immediate neonatal resuscitation for newborns with low Apgar scores may help to prevent CP in children.


The author would like to thank Eleni Tesfaye Tegegne and Mekibib Kassa Tessema from the University of Gondar both of them worked as critical appraisers and Debark University, College of Health Science, for assisting me in doing this systematic review.


There are no conflicts of interest stated by the author.


There was no financing available for this review.


Ethics approval and consent to participate are not applicable.


  1. Bax MC. Terminology and classification of cerebral palsy. Dev Med Child Neurol. 1964;6(3):295–7. https://doi.org/10.1111/j.1469-8749.1964.tb10791.x. PMID:14155190.
  2. Paneth N, Hong T, Korzeniewski S. The descriptive epidemiology of cerebral palsy. Clin Perinatol. 2006;33(2):251–67. https://doi.org/10.1016/j.clp.2006.03.011. PMID:16765723.
  3. Mutch L, Alberman E, Hagberg B, Kodama K, Perat MV. Cerebral palsy epidemiology: Where are we now and where are we going? Dev Med Child Neurol. 1992;34(6):547–51. https://doi.org/10.1111/j.1469-8749.1992.tb11479.x. PMID:1612216.
  4. Arneson CL, Durkin MS, Benedict RE, Kirby RS, Yeargin-Allsopp M, Van Naarden Braun K, et al. Prevalence of cerebral palsy: autism and developmental disabilities monitoring network, three sites, United States, 2004. Disabil Health J. 2009;2(1):45–8. https://doi.org/10.1016/j.dhjo.2008.08.001. PMID:21122742.
  5. Bhasin TK, Brocksen S, Avchen RN, Van Naarden Braun K. Prevalence of four developmental disabilities among children aged 8 years—Metropolitan Atlanta Developmental Disabilities Surveillance Program, 1996 and 2000. MMWR Surveill Summ. 2006;55(1):1–9. PMID:16437058.
  6. Johnson A. Prevalence and characteristics of children with cerebral palsy in Europe. Dev Med Child Neurol. 2002;44(9):633–40. https://doi.org/10.1017/S0012162201002675. PMID:12227618.
  7. Winter S, Autry A, Boyle C, Yeargin-Allsopp M. Trends in the prevalence of cerebral palsy in a population-based study. Pediatrics. 2002;110(6):1220–5. https://doi.org/10.1542/peds.110.6.1220. PMID:12456922.
  8. Adding E, Roebroeck ME, Stam HJ. e epidemiology of cerebral palsy: incidence, impairments and risk factors, Disabil Rehabil. 2006;28:183–91. https://doi.org/10.1080/09638280500158422. PMID:16467053.
  9. Hirtz D, Thurman DJ, Gwinn-Hardy K, Mohamed M, Chaudhuri AR, Zalutsky R. How common are the “common” neurologic disorders? Neurology. 2007;68(5):326–37. https://doi.org/10.1212/01.wnl.0000252807.38124.a3. PMID:17261678.
  10. Bendale AG, Baviskar SP. A study of clinical profile and factors associated with Int J Physiother 2020; 7(2):103, cerebral palsies in children at a tertiary health care center. Int J Pediatr. 2017;2(2):8–11.
  11. Saadi HR, Sutan R, Dhaher A, Alshaham SA. Maternal and fetal risk factors of cerebral palsy among Iraqi children: a case control study. J Prev Med (Wilmington). 2012;2(3):350–8.
  12. Pritchard MA, Colditz PB, Cartwright D, Gray PH, Tudehope D, Beller E. Risk determinants in early intervention use during the first postnatal year in children born very preterm. BMC Pediatr. 2013;13(1):201. https://doi.org/10.1186/1471-2431-13-201. PMID:24304976.
  13. O’Callaghan M, MacLennan A. Cesarean delivery and cerebral palsy: a systematic review and meta-analysis. Obstet Gynecol. 2013;122(6):1169–75. https://doi.org/10.1097/AOG.0000000000000020. PMID:24201683.
  14. Stoknes M, Andersen GL, Elkamil AI, Irgens LM, Skranes J, Salvesen KÅ, et al. The effects of multiple pre- and perinatal risk factors on the occurrence of cerebral palsy. A Norwegian register based study. Eur J Paediatr Neurol. 2012;16(1):56–63. https://doi.org/10.1016/j.ejpn.2011.10.004. PMID:22104566.
  15. Trønnes H, Wilcox AJ, Lie RT, Markestad T, Moster D. Risk of cerebral palsy in relation to pregnancy disorders and preterm birth: a national cohort study. Dev Med Child Neurol. 2014;56(8):779–85. https://doi.org/10.1111/dmcn.12430. PMID:24621110.
  16. Kułak W, Okurowska-Zawada B, Sienkiewicz D, Paszko-Patej G, Krajewska-Kułak E. Risk factors for cerebral palsy in term birth infants. Adv Med Sci. 2010;55(2):216–21. https://doi.org/10.2478/v10039-010-0030-7. PMID:20688615.
  17. Birth weight in premature babies is another risk factor Surveillance of Cerebral Palsy in Europe. Prevalence and characteristics of children with cerebral palsy in Europe. Dev Med Child Neurol. 2002;44(9):633–40. https://doi.org/10.1111/j.1469-8749.2002.tb00848.x
  18. Oskoui M, Coutinho F, Dykeman J, Jetté N, Pringsheim T. An update on the prevalence of cerebral palsy: a systematic review and meta-analysis. Dev Med Child Neurol. 2013;55(6):509–19. https://doi.org/10.1111/dmcn.12080. PMID:23346889.
  19. Blair E, Stanley F. When can cerebral palsy be prevented? The generation of causal hypotheses by multivariate analysis of a case-control study. Paediatr. Perinat. Epidemiol. 1993;7(3):272–301. https://doi.org/10.1111/j.1365-3016.1993.tb00405.x. PMID:8378170.
  20. Thorngren-Jerneck K, Herbst A. Perinatal factors associated with cerebral palsy in children born in Sweden. Obstet Gynecol. 2006;108(6):1499–505. https://doi.org/10.1097/01.AOG.0000247174.27979.6b. PMID:17138786.
  21. Jarvis S, Glinianaia SV, Torrioli MG, Platt MJ, Miceli M, Jouk PS, et al. Surveillance of Cerebral Palsy in Europe (SCPE) collaboration of European Cerebral Palsy Registers. Cerebral palsy and intrauterine growth in single births: European collaborative study. Lancet. 2003;362(9390):1106–11. https://doi.org/10.1016/S0140-6736(03)14466-2. PMID:14550698.
  22. Topp M, Huusom LD, Langhoff-Roos J, Delhumeau C, Hutton JL, Dolk H, SCPE Collaborative Group. Multiple birth and cerebral palsy in Europe: a multicenter study. Acta Obstet Gynecol Scand. 2004;83(6):548–53. https://doi.org/10.1111/j.0001-6349.2004.00545.x. PMID:15144336.
  23. Tsige S, Moges A, Mekasha A, Abebe W, Forssberg H. Cerebral palsy in children: subtypes, motor function and associated impairments in Addis Ababa, Ethiopia. BMC Pediatr. 2021;21(1):544. https://doi.org/10.1186/s12887-021-03026-y. PMID:34861837.
  24. Ekanem PE, Nyaga AC, Tsegay N, Ebuy H, Imbusi EA, Ekanem R, et al. Determinants of cerebral palsy in pediatric patients in Northern Ethiopia: a hospital-based study. Neurol Res Int. 2021;2021:9993912. https://doi.org/10.1155/2021/9993912. PMID:34966561.
  25. McIntyre S, Blair E, Badawi N, Keogh J, Nelson KB. Antecedents of cerebral palsy and perinatal death in term and late preterm singletons. Obstet Gynecol. 2013;122(4):869–77. https://doi.org/10.1097/AOG.0b013e3182a265ab. PMID:24084547.
  26. Eyong KI, Ekanem E, Aside A. Challenges of caregivers of children with cerebral palsy in a developing country. Int J Contemp Pediatrics. 2017;4(4):1128–31. https://doi.org/10.18203/2349-3291.ijcp20172656
  27. Kakooza-Mwesige A, Andrews C, Peterson S, Mangen FW, Eliasson AC, Forssberg H. Prevalence of cerebral palsy in Uganda: a population-based study. Lancet Glob Health. 2017; 5.
  28. Monokwane B, Johnson A, Gambrah-Sampaney C et al., Risk factors for cerebral palsy in children in Botswana. Pediatr Neurol. 2017;77:73–7.
  29. Sell E, Muñoz F. Commentary neonatal encephalopathy: case definition and guidelines for data collection, analysis, and presentation of maternal immunization safety data. Vaccine. 2017; 35(48Part A):6501–6505.
  30. Stavsky M, Mor O, Mastrolia SA, Greenbaum S, Than NG, Erez Z. Cerebral palsy-trend in epidemiology and recent development in prenatal mechanisms of disease, treatment and prevention. Front. Pediatr. 2017;5:21. https://doi.org/10.3389/fped.2017.00021
  31. Tatavarti SR, Arimilli V, Subbalakshmi TDP. Cerebral palsy: antenatal risk factors. J Evol Med Dental Sci 2015;4(37):6512–16. https://doi.org/10.14260/jemds/2015/944
  32. Nottidge VA, Okogbo ME. Cerebral palsy in Ibadan, Nigeria. Dev Med Child Neurol. 1991;33(3):241–5. https://doi.org/10.1111/j.1469-8749.1991.tb05113.x. PMID:2026281.
  33. Monokwane B, Johnson A, Gambrah-Sampaney C, Khurana E, Baier J, Baranov E, et al. Risk factors for cerebral palsy in children in Botswana. Pediatr Neurol. 2017;77:73–7. https://doi.org/10.1016/j.pediatrneurol.2017.07.014. PMID:29074060.
  34. Bearden DR, Monokwane B, Khurana E, Baier J, Baranov E, Westmoreland K, et al. Pediatric cerebral palsy in Botswana: etiology, outcomes, and comorbidities. Pediatr Neurol. 2016;59:23–9. https://doi.org/10.1016/j.pediatrneurol.2016.03.002. PMID:27114082.
  35. Kisanga AO, Verma A, Bhaskaran AA, Elangovan M. Prevalence of cerebral palsy in children under five in and around dar-Es-salaam. IMTU Med J. 2012;3.
  36. Atiemo E, Onike R, Badoe E. Classification and risk factors for cerebral palsy in the korle bu teaching hospital, accra: a case-control study. Paediatrics; 2015:135.
  37. Bendale AG, Baviskar SP. A study of clinical profile and factors associated with Int J Physiother 2020;7(2):103; cerebral palsy in children at tertiary health care center. Int J Pediatr. 2017;2(2):8–11.
  38. Nelson KB, Ellenberg JH. Predictors of low and very low birth weight and the relation of these to cerebral palsy. JAMA. 1985;254(11):1473–9. https://doi.org/10.1001/jama.1985.03360110063025. PMID:4032650.
  39. Torfs CP, van den Berg B, Oechsli FW, Cummins S. Prenatal and perinatal factors in the etiology of cerebral palsy. J Pediatr. 1990;116(4):615–9. https://doi.org/10.1016/S0022-3476(05)81615-4. PMID:2181101.
  40. Stanley FJ, Blair E, Alberman E. Cerebral palsies: epidemiology and causal pathways. Clinics in Developmental Medicine No 151. London: MacKeith Press; 2000.
  41. Num Zupan V, Gonzalez P, Lacaze-Masmonteil T, et al. Periventricular leukomalacia: risk factors revisited. Dev Med Child Neurol. 1996;38:1061–1067.
  42. Kułak W, Sobaniec W, Okurowska-Zawada B, et al. Antenatal, intrapartum and neonatal risk factors for cerebral palsy in children in Podlaskie Province NeurologIaDzIecIêca 18/2009, nr 36.
  43. Chen D, Huang M, Yin Y, Gui D, Gu Y, Zhuang T, et al. Risk factors of cerebral palsy in children: a systematic review and meta-analysis. Transl Pediatr. 2022;11(4):556–64. https://doi.org/10.21037/tp-22-78. PMID:35558974.
  44. Garne E, Dolk H, Krägeloh-Mann I, Holst Ravn S, Cans C; SCPE Collaborative Group. Cerebral palsy and congenital malformations. Eur J Paediatr Neurol. 2008;12(2):82–8. https://doi.org/10.1016/j.ejpn.2007.07.001. PMID:17881257.
  45. Spinillo A, Capuzzo E, Orcesi S, Stronati M, Di Mario M, Fazzi E. Antenatal and delivery risk factors simultaneously associated with neonatal death and cerebral palsy in preterm infants. Early Hum Dev. 1997;48(1–2):81–91. https://doi.org/10.1016/S0378-3782(96)01838-5. PMID:9131309.
  46. A FB et le risk factors associated with cerebral palsy instituto nuevo amanecer a.b.p., Nuevo León, México. https://www.aacpdm.org/UserFiles/file/DP2-Barron.pdf
  47. Wolf-Vereecken MJ. Neurodevelopmental outcome in high-risk Zimbabwean Neonates. Katholieke Universiteit Leuven: Thesis; 1997.
  48. Póo Argüelles P. Parálisis cerebral infantil. Asociación Española de Pediatría; 2008. https://www.aeped.es/sites/default/files/documentos/36-pci.pdf
  49. Khandaker G, Muhit M, Karim T, Smithers-Sheedy H, Novak I, Jones C, et al. Epidemiology of cerebral palsy in Bangladesh: a population-based surveillance study. Dev Med Child Neurol. 2019;61(5):601–9. https://doi.org/10.1111/dmcn.14013. PMID:30394528.
  50. Eunson P. Aetiology and epidemiology of cerebral palsy. Paediatr Child Health. 2012;22(9):361–66.
  51. Murphy DJ, Sellers S, MacKenzie IZ, Yudkin PL, Johnson AM. Case-control study of antenatal and intrapartum risk factors for cerebral palsy in very preterm singleton babies. Lancet. 1995;346(8988):1449–54. https://doi.org/10.1016/S0140-6736(95)92471-X. PMID:7490990.
  52. 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):271–7. https://doi.org/10.1111/j.1651-2227.2001.tb00303.x. PMID:11332166.
  53. Blair E, Stanley F. Issues in the classification and epidemiology of cerebral palsy. Ment Retard Dev Disabil Res Rev. 2002;3(2):184–93. https://doi.org/10.1002/(SICI)1098-2779(1997)3:2<184::AID-MRDD10>3.0.CO;2-R.
  54. Hagberg B, Hagberg G, Olow I. The changing panorama of cerebral palsy in Sweden. VI. Prevalence and origin during the birth year period 1983–1986. Acta Paediatr. 1993;82(4):387–93. https://doi.org/10.1111/j.1651-2227.1993.tb12704.x. PMID:8318808.
  55. Stanley FJ, Watson L. Trends in perinatal mortality and cerebral palsy in Western Australia, 1967 to 1985. BMJ. 1992;304(6843):1658–63. https://doi.org/10.1136/bmj.304.6843.1658. PMID:1633518.
  56. Kuak P. Selected risk factors for spastic cerebral palsy in a retrospective hospital–based case control study. Prog Health Sci. 2014;4(2):7–13.
  57. Martinez et al, PARÁLISIS CEREBRAL Prevalence of risk factors for cerebral palsy in two centers in Popayán.
  58. Zhakupova MN, et al. Assessment of the main risk factors of development of children’s cerebral pals Revista Latinoamericana de Hipertensión, 2019;14(4). ISSN: 1856–4550.
  59. Soumya V, Madhavi KV, Madhavi BD. A study on maternal and perinatal risk factors of cerebral palsy among children attending a cerebral palsy clinic in Visakhapatnam. Int J Community Med Public Health. 2018;5(1):317–21. https://doi.org/10.18203/2394-6040.ijcmph20175805.
  60. Obaidul H, Ehsanur R, Mohammad HR. Antenatal risk factors of children with cerebral palsy. Biomed J Sci Tech Res. 2018;4(2). BJSTR.MS.ID.001021. 10.26717/BJSTR.2018.04.001021
  61. 1C. Hemachithra et al. Association of risk factors of cerebral palsy—a matched case control study. Int J Physiother. 2020;7(2):99–103.
  62. MV da Silva Peixoto et al. Risk factors for cerebral palsy in Brazilian Children. A case-control study research. Soc Dev. 2021;10(5):e35710515075.
  63. Jöud A, Sehlstedt A, Källén K, Westbom L, Rylander L. Associations between antenatal and perinatal risk factors and cerebral palsy: a Swedish cohort study. BMJ Open. 2020;10(8):e038453. https://doi.org/10.1136/bmjopen-2020-038453. PMID:32771990.
  64. Singhi PD, Ray M, Suri G. Clinical spectrum of cerebral palsy in north India—an analysis of 1,000 cases. J Trop Pediatr. 2002;48(3):162–6. https://doi.org/10.1093/tropej/48.3.162. PMID:12164600
  65. Karumuna JM, Mgone CS. Cerebral palsy in Dar Es Salaam. Cent Afr J Med. 1990;36(1):8–10. PMID:2397497.
  66. Nelson KB, Grether JK. Causes of cerebral palsy. Curr Opin Pediatr. 1999;11(6):487–91. https://doi.org/10.1097/00008480-199912000-00002. PMID:10590904.
  67. Scher AI, Petterson B, Blair E, Ellenberg JH, Grether JK, Haan E, et al. The risk of mortality or cerebral palsy in twins: a collaborative population-based study. Pediatr Res. 2002;52(5):671–81. https://doi.org/10.1203/00006450-200211000-00011. PMID:12409512.
  68. Gaffney G, Flavell V, Johnson A, Squier M, Sellers S. Cerebral palsy and neonatal encephalopathy. Arch Dis Child Fetal Neonatal Ed. 1994;70(3):F195–200. https://doi.org/10.1136/fn.70.3.F195. PMID:7802763.
  69. Badawi N, Felix JF, Kurinczuk JJ, Dixon G, Watson L, Keogh JM, et al. Cerebral palsy following term newborn encephalopathy: a population-based study. Dev Med Child Neurol. 2005;47(5):293–8. https://doi.org/10.1017/S0012162205000575. PMID:15892370.
  70. Dolk H, Pattenden S, Johnson A. Cerebral palsy, low birthweight and socio-economic deprivation: inequalities in a major cause of childhood disability. Paediatr Perinat Epidemiol. 2001;15(4):359–63. https://doi.org/10.1046/j.1365-3016.2001.00351.x. PMID:11703684.
  71. 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(3):191–5. https://doi.org/10.1136/jech.44.3.191. PMID:2148770.
  72. Croen LA, Grether JK, Curry CJ, Nelson KB. Congenital abnormalities among children with cerebral palsy: more evidence for prenatal antecedents. J Pediatr. 2001;138(6):804–10. https://doi.org/10.1067/mpd.2001.114473. PMID:11391320.
  73. Nelson KB, Ellenberg JH. Antecedents of cerebral palsy. Multivariate analysis of risk. N Engl J Med. 1986;315(2):81–6. https://doi.org/10.1056/NEJM198607103150202. PMID:3724803.
  74. Palmer L, Blair E, Petterson B, Burton P. Antenatal antecedents of moderate and severe cerebral palsy. Paediatr Perinat Epidemiol. 1995;9(2):171–84. https://doi.org/10.1111/j.1365-3016.1995.tb00132.x. PMID:7596894.
  75. Krägeloh-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(5):379–97. https://doi.org/10.1111/j.1469-8749.1995.tb12022.x. PMID:7768338.
  76. Steinlin M, Good M, Martin E, Bänziger O, Largo RH, Boltshauser E. Congenital hemiplegia: morphology of cerebral lesions and pathogenetic aspects from MRI. Neuropediatrics. 1993;24(4):224–9. https://doi.org/10.1055/s-2008-1071545. PMID:8232782.
  77. Truwit CL, Barkovich AJ, Koch TK, Ferriero DM. Cerebral palsy: MR findings in 40 patients. AJNR Am J Neuroradiol. 1992;13(1):67–78. PMID:1595496.
  78. Topp M, Langhoff-Roos J, Uldall P. Preterm birth and cerebral palsy. Predictive value of pregnancy complications, mode of delivery, and Apgar scores. Acta Obstet Gynecol Scand. 1997;76(9):843–8. https://doi.org/10.3109/00016349709024363. PMID:9351410.
  79. Lee J, Croen LA, Backstrand KH, Yoshida CK, Henning LH, Lindan C, et al. Maternal and infant characteristics associated with perinatal arterial stroke in the infant. JAMA. 2005;293(6):723–9. https://doi.org/10.1001/jama.293.6.723. PMID:15701914.
  80. Walstab J, Bell R, Reddihough D, Brennecke S, Bessell C, Beischer N. Antenatal and intrapartum antecedents of cerebral palsy: a case-control study. Aust N Z J Obstet Gynaecol. 2002;42(2):138–46. https://doi.org/10.1111/j.0004-8666.2002.00138.x. PMID:12069139.
  81. Powell TG, Pharoah PO, Cooke RW, Rosenbloom L. Cerebral palsy in low-birthweight infants. I. Spastic hemiplegia: associations with intrapartum stress. Dev Med Child Neurol. 1988;30(1):11–8. https://doi.org/10.1111/j.1469-8749.1988.tb04721.x. PMID:3371563.
  82. Stanley FJ. Prenatal determinants of motor disorders. Acta Paediatr Suppl. 1997;422 S422:92–102. https://doi.org/10.1111/j.1651-2227.1997.tb18355.x. PMID:9298803.
  83. Himmelmann K, Hagberg G, Beckung E, Hagberg B, Uvebrant P. The changing panorama of cerebral palsy in Sweden. IX. Prevalence and origin in the birth-year period 1995–1998. Acta Paediatr. 2005;94(3):287–94. https://doi.org/10.1111/j.1651-2227.2005.tb03071.x. PMID:16028646.
  84. Eastman NJ, Deleon M. The etiology of cerebral palsy. Am J Obstet Gynecol. 1955;69(5):950–61. https://doi.org/10.1016/0002-9378(55)90094-6. PMID:14361524.
  85. Grether JK, Nelson KB, Emery ES 3rd, Cummins SK. Prenatal and perinatal factors and cerebral palsy in very low birth weight infants. J Pediatr. 1996;128(3):407–14. https://doi.org/10.1016/S0022-3476(96)70292-5. PMID:8774515.
  86. Spinillo A, Capuzzo E, Cavallini A, Stronati M, De Santolo A, Fazzi E. Preeclampsia, preterm delivery and infant cerebral palsy. Eur J Obstet Gynecol Reprod Biol. 1998a;77(2):151–5. https://doi.org/10.1016/S0301-2115(97)00246-7. PMID:9578271.
  87. Gilles MT, Blair E, Watson L, Badawi N, Alessandri L, Dawes V, et al. Trauma in pregnancy and cerebral palsy: Is there a link? Med J Aust. 1996;164(8):500–1. https://doi.org/10.5694/j.1326-5377.1996.tb122138.x. PMID:8614347.
  88. Nelson KB, Willoughby RE. Infection, inflammation and the risk of cerebral palsy. Curr Opin Neurol. 2000;13(2):133–9. https://doi.org/10.1097/00019052-200004000-00004. PMID:10987569.
  89. Polivka BJ, Nickel JT, Wilkins JR 3rd. Urinary tract infection during pregnancy: a risk factor for cerebral palsy? J Obstet Gynecol Neonatal Nurs. 1997;26(4):405–13. https://doi.org/10.1111/j.1552-6909.1997.tb02722.x. PMID:9252888.
  90. Spinillo A, Capuzzo E, Stronati M, Ometto A, De Santolo A, Acciano S. Obstetric risk factors for periventricular leukomalacia among preterm infants. Br J Obstet Gynaecol. 1998b;105(8):865–71. https://doi.org/10.1111/j.1471-0528.1998.tb10231.x. PMID:9746379.
  91. Lagunju IA, Okafor OO. An analysis of disorders seen at the Paediatric Neurology Clinic, University College Hospital, Ibadan, Nigeria. West Afr J Med. 2009;28(1):38–42. https://doi.org/10.4314/wajm.v28i1.48424. PMID:19662744.
  92. Mukhtar-Yola M, Iliyasu Z. A review of neonatal morbidity and mortality in Aminu Kano Teaching Hospital, northern Nigeria. Trop Doct. 2007;37(3):130–2. https://doi.org/10.1258/004947507781524683. PMID:17716492.
  93. Nelson KB. Causative factors in cerebral palsy. Clin Obstet Gynecol. 2008;51(4):749–62. https://doi.org/10.1097/GRF.0b013e318187087c. PMID:18981800.
  94. Nelson KB, Ellenberg JH. Apgar scores as predictors of chronic neurologic disability. Pediatrics. 1981;68(1):36–44. https://doi.org/10.1542/peds.68.1.36. PMID:7243507.
  95. van de Riet JE, Vandenbussche FP, Le Cessie S, Keirse MJ. Newborn assessment and long-term adverse outcome: a systematic review. Am J Obstet Gynecol. 1999;180(4):1024–9. https://doi.org/10.1016/S0002-9378(99)70676-9. PMID:10203673.
  96. Moster D, Lie RT, Irgens LM, 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(6):798–803. https://doi.org/10.1067/mpd.2001.114694. PMID:11391319.
  97. Murphy DJ, Hope PL, Johnson A. Neonatal risk factors for cerebral palsy in very preterm babies: case-control study. BMJ. 1997;314(7078):404–8. https://doi.org/10.1136/bmj.314.7078.404. PMID:9040385.
  98. Comans T, Mihala G, Sakzewski L, Boyd RN, Scuffham P. The cost-effectiveness of a web-based multimodal therapy for unilateral cerebral palsy: the Mitii randomized controlled trial. Dev Med Child Neurol. 2017;59(7):756–61. https://doi.org/10.1111/dmcn.13414. PMID:28247406.
  99. Glass HC, Bonifacio SL, Chau V, Glidden D, Poskitt K, Barkovich AJ, et al. Recurrent postnatal infections are associated with progressive white matter injury in premature infants. Pediatrics. 2008;122(2):299–305. https://doi.org/10.1542/peds.2007-2184. PMID:18676547.
  100. Olusanya BO, Somefun AO. Sensorineural hearing loss in infants with neonatal jaundice in Lagos: a community-based study. Ann Trop Paediatr. 2009;29(2):119–28. https://doi.org/10.1179/146532809X440734. PMID:19460265.
  101. Roze E, Benders MJ, Kersbergen KJ, van der Aa NE, Groenendaal F, van Haastert IC, et al. Neonatal DTI early after birth predicts motor outcome in preterm infants with periventricular hemorrhagic infarction. Pediatr Res. 2015;78(3):298–303. https://doi.org/10.1038/pr.2015.94 PMID:25978802.
  102. Fletcher NA, Foley J. Parental age, genetic mutation, and cerebral palsy. J Med Genet. 1993;30(1):44–6. https://doi.org/10.1136/jmg.30.1.44. PMID:8423607.
  103. Pinto-Martin JA, Cnaan A, Zhao H. Short interpregnancy interval and the risk of disabling cerebral palsy in a low birth weight population. J Pediatr. 1998;132(5):818–21. https://doi.org/10.1016/S0022-3476(98)70310-5 PMID:9602192.
  104. Reddihough DS, Collins KJ. The epidemiology and causes of cerebral palsy. Aust J Physiother. 2003;49(1):7–12. https://doi.org/10.1016/S0004-9514(14)60183-5. PMID:12600249
  105. Ku ak W, Sobaniec W, Okurowska-Zawada B, Sienkiewicz D, Paszko-Patej G. Antenatal, intrapartum and neonatal risk factors for cerebral palsy in children in Podlaskie Province. Neurol Dziec. 2009;18(36):19–24.
  106. McIntyre S, Taitz D, Keogh J, Goldsmith S, Badawi N, Blair E. A systematic review of risk factors for cerebral palsy in children born at term in developed countries. Dev Med Child Neurol. 2013;55(6):499–508. https://doi.org/10.1111/dmcn.12017. PMID:23181910.
  107. Linsell L, Malouf R, Morris J, Kurinczuk JJ, Marlow N. Prognostic factors for cerebral palsy and motor impairment in children born very preterm or very low birthweight: a systematic review. Dev Med Child Neurol. 2016;58(6):554–69. https://doi.org/10.1111/dmcn.12972. PMID:26862030.
  108. Ahlin K, Himmelmann K, Hagberg G, Kacerovsky M, Cobo T, Wennerholm UB, et al. Non-infectious risk factors for different types of cerebral palsy in term-born babies: a population-based, case-control study. BJOG. 2013;120(6):724–31. https://doi.org/10.1111/1471-0528.12164. PMID:23418811.
  109. Goldsmith S, Mcintyre S, Badawi N, Hansen M. Cerebral palsy after assisted reproductive technology: a cohort study. Dev Med Child Neurol. 2018;60(1):73–80. https://doi.org/10.1111/dmcn.13577. PMID:28980316.
  110. 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(8):946–51. https://doi.org/10.1111/j.1651-2227.2002.tb02860.x. PMID:12222720.
  111. Amin-Zaki L, Majeed MA, Elhassani SB, Clarkson TW, Greenwood MR, Doherty RA. Prenatal methylmercury poisoning. Clinical observations over five years. Am J Dis Child. 1979;133(2):172–7. https://doi.org/10.1001/archpedi.1979.02130020064013. PMID:84530.
  112. Hemminki K, Li X, Sundquist K, et al. Familial risks for common diseases: etiologic clues and guidance to gene identification. Mutat Res. 2008 [Epub ahead of print, January 12]. https://doi.org/10.1016/j.mrrev.2008.01.002.
  113. Gibson CS, MacLennan AH, Goldwater PN, Haan EA, Priest K, Dekker GA, South Australian Cerebral Palsy Research Group. The association between inherited cytokine polymorphisms and cerebral palsy. Am J Obstet Gynecol. 2006;194(3):674.e1–11. https://doi.org/10.1016/j.ajog.2006.01.093. PMID:16522396.
  114. Nelson KB, Dambrosia JM, Iovannisci DM, Cheng S, Grether JK, Lammer E. Genetic polymorphisms and cerebral palsy in very preterm infants. Pediatr Res. 2005;57(4):494–9. https://doi.org/10.1203/01.PDR.0000156477.00386.E7. PMID:15718364.
  115. O’Shea TM, Klinepeter KL, Dillard RG. Prenatal events and the risk of cerebral palsy in very low birth weight infants. Am J Epidemiol. 1998;147(4):362–9. https://doi.org/10.1093/oxfordjournals.aje.a009458. PMID:9508103.
  116. Singhi P, Saini AG. Changes in the clinical spectrum of cerebral palsy over two decades in North India—an analysis of 1212 cases. J Trop Pediatr. 2013;59(6):434–40. https://doi.org/10.1093/tropej/fmt035. PMID:23783583.
  117. Stanley FJ, Sim M, Wilson G, Worthington S. The decline in congenital rubella syndrome in Western Australia: an impact of the school girl vaccination program? Am J Public Health. 1986;76(1):35–7. https://doi.org/10.2105/AJPH.76.1.35. PMID:3940451.
  118. Hagberg H, Mallard C. Antenatal brain injury: aetiology and possibilities of prevention. Semin Neonatol. 2000;5(1):41–51. https://doi.org/10.1053/siny.1999.0114. PMID:10802749.
  119. O’Shea TM, Klinepeter KL, Meis PJ, Dillard RG. Intrauterine infection and the risk of cerebral palsy in very low-birthweight infants. Paediatr Perinat Epidemiol. 1998;12(1):72–83. https://doi.org/10.1111/j.1365-3016.1998.00081.x. PMID:9483618.
  120. Piper JM, Newton ER, Berkus MD, Peairs WA. Meconium: a marker for peripartum infection. Obstet Gynecol. 1998;91(5 Pt 1):741–5. PMID:9572222.
  121. Gladstone M, Oliver C, Van den Broek N. Survival, morbidity, growth and developmental delay for babies born preterm in low and middle income countries—a systematic review of outcomes measured. PLoS One. 2015;10(3):e0120566. https://doi.org/10.1371/journal.pone.0120566. PMID:25793703.
  122. Coorssen EA, Msall ME, Duffy LC. Multiple minor malformations as a marker for prenatal etiology of cerebral palsy. Dev Med Child Neurol. 1991;33(8):730–6. https://doi.org/10.1111/j.1469-8749.1991.tb14952.x. PMID:1916028.
  123. Nelson KB, Leviton A. How much of neonatal encephalopathy is due to birth asphyxia? Am J Dis Child. 1991;145(11):1325–31. PMID:1835281.
  124. Amiel-Tison C, Pettigrew AG. Adaptive changes in the developing brain during intrauterine stress. Brain Dev. 1991;13(2):67–76. https://doi.org/10.1016/S0387-7604(12)80109-4. PMID:1892222.
  125. Ridker PM, Miletich JP, Hennekens CH, Buring JE. Ethnic distribution of factor V Leiden in 4047 men and women. Implications for venous thromboembolism screening. JAMA. 1997;277(16):1305–7. https://doi.org/10.1001/jama.1997.03540400055031. PMID:9109469.
  126. 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(3):372–5. https://doi.org/10.1002/ana.410420316. PMID:9307261.
  127. Nelson KB, Grether JK. Potentially asphyxiating conditions and spastic cerebral palsy in infants of normal birth weight. Am J Obstet Gynecol. 1998b;179(2):507–13. https://doi.org/10.1016/S0002-9378(98)70387-4. PMID:9731861.
  128. Williams K, Hennessy E, Alberman E. Cerebral palsy: effects of twinning, birthweight, and gestational age. Arch Dis Child Fetal Neonatal Ed. 1996;75(3):F178–82. https://doi.org/10.1136/fn.75.3.F178. PMID:8976683.
  129. Pharoah POD and Cooke RWI. A hypothesis for the aetiology of spastic cerebral palsy—the vanishing twin. Developmental Medicine and Child Neurology. 1997;39:292–296, 132.
  130. Bangash AS et al. Risk factors and types of cerebral palsy. JPMA. 2014;64:103.
  131. Pharoah PO, Buttfield IH, Hetzel BS. Neurological damage to the fetus resulting from severe iodine deficiency during pregnancy. Lancet. 1971;1(7694):308–10. https://doi.org/10.1016/S0140-6736(71)91040-3. PMID:4100150.
  132. Curry CJ, Bhullar S, Holmes J, Delozier CD, Roeder ER, Hutchison HT. Risk factors for perinatal arterial stroke: a study of 60 mother-child pairs. Pediatr Neurol. 2007;37(2):99–107. https://doi.org/10.1016/j.pediatrneurol.2007.04.007. PMID:17675024.
  133. Kuroda MM, Weck ME, Sarwark JF, Hamidullah A, Wainwright MS. Association of apolipoprotein E genotype and cerebral palsy in children. Pediatrics. 2007;119(2):306–13. https://doi.org/10.1542/peds.2006-1083. PMID:17272620.
  134. Gibson CS, Maclennan AH, Dekker GA, Goldwater PN, Sullivan TR, Munroe DJ, et al. Candidate genes and cerebral palsy: a population-based study. Pediatrics. 2008;122(5):1079–85. https://doi.org/10.1542/peds.2007-3758. PMID:18977990.
  135. Badawi N, Kurinczuk JJ, Keogh JM, Alessandri LM, O’Sullivan F, Burton PR, et al. Antepartum risk factors for newborn encephalopathy: the Western Australian case-control study. BMJ. 1998;317(7172):1549–53. https://doi.org/10.1136/bmj.317.7172.1549. PMID:9836652.
  136. Haddow JE, Palomaki GE, Allan WC, Williams JR, Knight GJ, Gagnon J, et al. Maternal thyroid deficiency during pregnancy and subsequent neuropsychological development of the child. N Engl J Med. 1999;341(8):549–55. https://doi.org/10.1056/NEJM199908193410801. PMID:10451459.
  137. Wasserman EE, Nelson K, Rose NR, et al. Maternal thyroid autoantibodies during the third trimester and hearing deficits in children: an epidemiologic assessment. Am J Epidemiol. 2007 [Epub ahead of print, December 21]. https://doi.org/10.1093/aje/kwm342
  138. Hasegawa J, Toyokawa S, Ikenoue T, Asano Y, Satoh S, Ikeda T, Maeda T. PLoS One. 2016;11(1):1–13. PMID:26821386.
  139. Wu YW, Colford JM Jr. Chorioamnionitis as a risk factor for cerebral palsy: a meta-analysis. JAMA. 2000;284(11):1417–24. https://doi.org/10.1001/jama.284.11.1417. PMID:10989405.
  140. Nelson KB, Grether JK. Can magnesium sulfate reduce the risk of cerebral palsy in very low birthweight infants? Pediatrics. 1995;95(2):263–9. https://doi.org/10.1542/peds.95.2.263. PMID:7838646.
  141. Schendel DE, Berg CJ, Yeargin-Allsopp M, Boyle CA, Decoufle P. Prenatal magnesium sulfate exposure and the risk for cerebral palsy or mental retardation among very low-birth-weight children aged 3 to 5 years. JAMA. 1996;276(22):1805–10. https://doi.org/10.1001/jama.1996.03540220029026. PMID:8946900.
  142. Willoughby RE Jr, Nelson KB. Chorioamnionitis and brain injury. Clin Perinatol. 2002;29(4):603–21. https://doi.org/10.1016/S0095-5108(02)00058-1. PMID:12516738.
  143. Michaud AP, Bauman NM, Burke DK, Manaligod JM, Smith RJ. Spastic diplegia and other motor disturbances in infants receiving interferon-alpha. Laryngoscope. 2004;114(7):1231–6. https://doi.org/10.1097/00005537-200407000-00017. PMID:15235352.
  144. Gladstone M, Annals of tropical paediatrics. 2010;30(3):181–96.
  145. Tonkonozhenko NL, Klitochenko GV, Krivonozhkina PS, Maliuzhinskaia NV, Lekarstvennyi vestnik. 2015;1(57):1–8.
  146. Ellis M, Shrestha L, Shrestha PS, Manandhar DS, Bolam AJ, L Costello AM. Clinical predictors of outcome following mild and moderate neonatal encephalopathy in term newborns in Kathmandu, Nepal. Acta Paediatr. 2001;90(3):316–22. https://doi.org/10.1111/j.1651-2227.2001.tb00311.x. PMID:11332174.
  147. Gladstone M. A review of the incidence and prevalence, types and aetiology of childhood cerebral palsy in resource-poor settings. Ann Trop Paediatr. 2010;30(3):181–96. https://doi.org/10.1179/146532810X12786388978481. PMID:20828451.
  148. Barkovich AJ, Truwit CL. Brain damage from perinatal asphyxia: correlation of MR findings with gestational age. AJNR Am J Neuroradiol. 1990;11(6):1087–96. PMID:2124034.
  149. Kuban KC, Leviton A. Cerebral palsy. N Engl J Med. 1994;330(3):188–95. https://doi.org/10.1056/NEJM199401203300308. PMID:8264743.
  150. Jacobsson B, Hagberg G. Antenatal risk factors for cerebral palsy. Best Pract Res Clin Obstet Gynaecol. 2004;18(3):425–36. https://doi.org/10.1016/j.bpobgyn.2004.02.011. PMID:15183137.
  151. 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(9):835–43. https://doi.org/10.1111/dmcn.12746. PMID:25808915.
  152. 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(6):CD012409. https://doi.org/10.1002/14651858.CD012409.pub2. PMID:29926474.
  153. Jacobs SE, Berg M, Hunt R, Tarnow-Mordi WO, Inder TE, Davis PG. Cooling for newborns with hypoxic ischaemic encephalopathy. Cochrane Database Syst Rev. 2013;2013(1):CD003311. https://doi.org/10.1002/14651858.CD003311.pub3 PMID:23440789
  154. Schmidt B, Roberts RS, Davis P, Doyle LW, Barrington KJ, Ohlsson A, et al. Caffeine for Apnea of Prematurity Trial Group. Long-term effects of caffeine therapy for apnea of prematurity. N Engl J Med. 2007;357(19):1893–902. https://doi.org/10.1056/NEJMoa073679. PMID:17989382.
  155. O’Shea TM, Kothadia JM, Klinepeter KL, Goldstein DJ, Jackson BG, Weaver RG 3rd, 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(1 Pt 1):15–21. https://doi.org/10.1542/peds.104.1.15. PMID:10390254.
  156. Watterberg KL, American Academy of Pediatrics. Committee on fetus and newborn. Policy statement—postnatal corticosteroids to prevent or treat bronchopulmonary dysplasia. Pediatrics. 2010;126(4):800–8. https://doi.org/10.1542/peds.2010-1534. PMID:20819899.
  157. Chollat C, Marret S. Magnesium sulfate and fetal neuroprotection: overview of clinical evidence. Neural Regen Res. 2018;13(12):2044–9. https://doi.org/10.4103/1673-5374.241441. PMID:30323118.
  158. 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 Company; 1998. pp. 31–5.
  159. Apak S, Korkmazlar U. Gelisimsel tani testleri. In: Apak S, editor. Gelisim Norolojisi. Istanbul, Turkey: Bayrak Matbaacilik; 1999. pp. 219–65.
  160. Matthews D. Cerebral palsy. In: Molnar G, Alexander M, editors. Pediatric Rehabilitation. Philadelphia, USA: Hanley&Belfus; 1999. pp. 193–2017.
  161. Christine C, Dolk H, Platt MJ, Colver A, Prasauskiene A, Krägeloh-Mann I, SCPE Collaborative Group. Recommendations from the SCPE collaborative group for defining and classifying cerebral palsy. Dev Med Child Neurol Suppl. 2007;109:35–8. PMID:17370480.

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Kaleab Tesfaye Tegegne. Determinants of cerebral palsy in children: systematic review. Sudan J Paed. 2023; 23(2): 126-144. doi:10.24911/SJP.106-1670589241

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Kaleab Tesfaye Tegegne. Determinants of cerebral palsy in children: systematic review. https://sudanjp.com//?mno=93371 [Access: April 25, 2024]. doi:10.24911/SJP.106-1670589241

AMA (American Medical Association) Style

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Kaleab Tesfaye Tegegne. Determinants of cerebral palsy in children: systematic review. Sudan J Paed. (2023), [cited April 25, 2024]; 23(2): 126-144. doi:10.24911/SJP.106-1670589241

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Kaleab Tesfaye Tegegne (2023) Determinants of cerebral palsy in children: systematic review. Sudan J Paed, 23 (2), 126-144. doi:10.24911/SJP.106-1670589241

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Kaleab Tesfaye Tegegne. 2023. Determinants of cerebral palsy in children: systematic review. Sudanese Journal of Paediatrics, 23 (2), 126-144. doi:10.24911/SJP.106-1670589241

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Kaleab Tesfaye Tegegne. "Determinants of cerebral palsy in children: systematic review." Sudanese Journal of Paediatrics 23 (2023), 126-144. doi:10.24911/SJP.106-1670589241

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Kaleab Tesfaye Tegegne. "Determinants of cerebral palsy in children: systematic review." Sudanese Journal of Paediatrics 23.2 (2023), 126-144. Print. doi:10.24911/SJP.106-1670589241

APA (American Psychological Association) Style

Kaleab Tesfaye Tegegne (2023) Determinants of cerebral palsy in children: systematic review. Sudanese Journal of Paediatrics, 23 (2), 126-144. doi:10.24911/SJP.106-1670589241

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