• Aetiology;
  • Cerebral palsy;
  • Epidemiology;
  • Gestational age;
  • Prevalence


  1. Top of page
  2. Abstract
  3. Introduction
  4. Method
  5. Results
  6. Discussion
  7. Acknowledgements
  8. References

Abstract Aim:  The aim of the study was to describe the prevalence and origin of cerebral palsy (CP), which is the tenth report from the western Swedish study.

Methods:  A population-based study covering 85 737 live births in the area in 1999–2002. Birth characteristics and neuroimaging findings were recorded, prevalence of CP was calculated and aetiology was analysed.

Results:  CP was found in 186 children. The crude prevalence was 2.18 per 1000 live births. The gestational age-specific prevalence for <28 gestational weeks was 55.6 per 1000 live births, whereas it was 43.7 for 28–31 weeks, 6.1 for 32–36 weeks and 1.43 per 1000 for >36 weeks. There was a female majority among children born at term and a male predominance in children born preterm. Hemiplegia accounted for 38%, diplegia for 32%, tetraplegia for 7%, whereas 17% had dyskinetic CP and 5% ataxia. Neuroimaging showed white-matter lesions in 31% and cortical/subcortical lesions in 29%. The aetiology was considered to be prenatal in 36%, peri/neonatal in 42%, whereas it remained unclassified in 21%.

Conclusion:  The decrease in CP prevalence observed since the 1980s had ceased. An increase in children born at term and in dyskinetic CP was found. In children born before 28 weeks of gestation, the prevalence decreased significantly. White-matter and cortical/subcortical lesions dominated on neuroimaging.


American College of Obstetricians and Gynecologists


central nervous system


cerebral palsy


computed tomography


hypoxic-ischaemic encephalopathy


large for gestational age


magnetic resonance imaging


neonatal mortality


perinatal mortality


Surveillance of Cerebral Palsy in Europe


standard deviation


small for gestational age


  1. Top of page
  2. Abstract
  3. Introduction
  4. Method
  5. Results
  6. Discussion
  7. Acknowledgements
  8. References

Cerebral palsy (CP) is an umbrella term for a group of conditions characterized by a motor impairment due to a malformation or lesion in the immature brain. The most recent definition, put forward by Bax et al. (1), also acknowledges the often accompanying impairments, relating to cognition, communication and sensation, for example, which sometimes over-shadow the motor problems.

Since 1971, the epidemiology of CP has been monitored continuously in the health care region of western Sweden (2), and the figures are currently based on data from 1908 children with CP born in 1954–2002. After an increase in prevalence in the 1970s, mostly due to the survival of more children born preterm with a motor impairment, the trend was reversed in the 1980s and we have observed a steadily decreasing trend since then (3). Within the panorama of CP, there has been a decrease in ever more preterm children with spastic diplegia (4), whereas the prevalence of hemiplegia and dyskinetic CP has shown a different pattern. The aim of this study, which is the tenth report on the prevalence and origin of CP from this register, was to describe the prevalence and background of CP in children born in 1999–2002 in a well-defined area of western Sweden.


  1. Top of page
  2. Abstract
  3. Introduction
  4. Method
  5. Results
  6. Discussion
  7. Acknowledgements
  8. References

The study comprised the counties of Västra Götaland, Jönköping and Halland, with a total population of 2.1 million inhabitants and slightly positive net migration. The study covered the birth-year period 1999–2002, in which 85 737 live births were recorded, 216 at <28 completed weeks of gestation, 503 at 28–31 weeks, 4598 at 32–36 weeks and 80 420 at >36 weeks of gestation. Children with CP were included if they were born in Sweden and lived in the study area on 31 December 2006. All the children had a diagnosis of CP verified at four to eight years of age by the local neuropaediatrician. In doubtful cases, a second diagnostic assessment was performed by the authors (KH, PU).

The definition of CP was that agreed at an international consensus meeting in Bethesda (1). The Swedish and internationally accepted classification of CP syndromes was applied (2,5), in parallel with the classification suggested by the Surveillance of Cerebral Palsy in Europe (SCPE) (6), where hemiplegia corresponds to unilateral spastic CP, and diplegia and tetraplegia are combined to create bilateral spastic CP. Extremely preterm birth was defined as birth occurring at <28 completed gestational weeks, very preterm at 28–31 weeks, moderately preterm at 32–36 weeks and birth at term at >36 weeks, based primarily on early ultrasound. If this information was not available, menstrual data were used. Prenatal referred to the period of pregnancy until the onset of labour resulting in delivery, perinatal to the period from the onset of labour until the seventh day of life, neonatal to the period up to day 28 and post-neonatal to the period from day 29 to 2 years of age. Maternal disorder was considered in the case of chronic disorder, pyelonephritis, or acute severe illness during pregnancy or fever of >38.5°C at delivery (7). Small for gestational age (SGA) was defined as a birth weight for gestational age of ≤−2SD, whereas large for gestational age (LGA) was defined as >2SD from the mean on a Swedish growth chart (8).

The aetiological classification was based on given clinical criteria, combined with available neuroimaging information (5). Obstetric and peri/neonatal data, as well as CP type, were derived from medical and habilitation records. The findings at computed tomography (CT) and magnetic resonance imaging (MRI) were classified, based on the description from the local radiologist or, when ambiguous, reinterpreted by a neuroradiologist into five categories: maldevelopment, white-matter lesions, cortical/subcortical lesions, basal ganglia/thalamus lesions, other findings and normal (9). Intra-cerebral haemorrhage was graded according to Papile et al. (10). Hypoxic-ischaemic encephalopathy (HIE) was considered in children born at ≥34 weeks of gestation in the presence of two or more of the following symptoms/signs: Apgar score <5 at 5 min, resuscitation/assisted ventilation and convulsions before day 3 (11). The following possible risk factors associated with CP were recorded: low Apgar score (<5 at 5 min), multiple birth, maternal disorder, SGA and LGA and applied in the unclassifiable group. The criteria of the American College of Obstetricians and Gynecologists (ACOG) (12) regarding intra-partal events severe enough to cause CP were applied in children born at ≥34 weeks of gestation (Table 1).

Table 1.   Criteria regarding intra-partal events severe enough to cause CP [American College of Obstetricians and Gynecologists (ACOG)]
Essential criteria
1. Evidence of a metabolic acidosis in foetal umbilical cord arterial blood obtained at delivery (pH <7.00 and base deficit ≥12 mmol/L).
2. Early onset of severe or moderate neonatal encephalopathy in infants born at 34 or more weeks of gestation.
3. Cerebral palsy of the spastic quadriplegic or dyskinetic type.
4. Exclusion of other identifiable aetiologies such as trauma, coagulation disorders, infectious conditions or genetic disorders.
Criteria that collectively suggest an intra-partum timing (within close proximity to labour and delivery, e.g. 0–48 h) but are non-specific to asphyxial insults
5. A sentinel (signal) hypoxic event occurring immediately before or during labour.
6. A sudden and sustained foetal bradycardia or the absence of foetal heart rate variability in the presence of persistent, late or variable decelerations, usually after a hypoxic sentinel event when the pattern was previously normal.
7. Apgar scores of 0–3 beyond 5 min.
8. Onset of multisystem involvement within 72 h of birth.
9. Early imaging study showing evidence of acute nonfocal cerebral abnormality.


The study was approved by the Ethics Committee at the Medical Faculty at Gothenburg University.


For the trend analyses, the ‘trend in proportions’ was used. For comparisons between groups, the chi-squared test was used. The level of significance was set at 0.05.


  1. Top of page
  2. Abstract
  3. Introduction
  4. Method
  5. Results
  6. Discussion
  7. Acknowledgements
  8. References

The average perinatal mortality (PNM) rate in 1999–2002 was 5.28 per 1000 births, and the average neonatal mortality rate was 2.18 per 1000 live births. The perinatal and neonatal mortality, together with CP prevalence during the birth years 1975–2002, are shown in Figure 1.


Figure 1.  Perinatal mortality (PNM) per 1000 births, neonatal mortality (NM) and prevalence of CP by 1000 live births in the birth years 1975–2002.

Download figure to PowerPoint

In the birth years 1999–2002, 186 children with CP were identified among the 85 737 live births in the study area. The crude mean prevalence was 2.18 per 1000 live births in the four-year cohort, 1.43 in children born at term and 0.75 in children born preterm. The decreasing trend since the 1980s had ceased in total CP and term CP, whereas the prevalence of preterm CP continued to fall. Nine children had an obvious post-neonatal cause of their CP. They are excluded in the following and reported separately. The crude prevalence is shown in Figure 2.


Figure 2.  Crude prevalence of CP per 1000 live births in the birth years 1959–2002.

Download figure to PowerPoint

Birth characteristics

Twelve children (7%) were born extremely preterm, 22 (12%) very preterm, 28 moderately preterm (16%) and 115 (65%) at term. Thirteen children (7%) had a birth weight of <1000 g, 16 (9%) a birth weight of 1000–1499 g, 31 (17%) a birth weight of 1500–2499 g and 118 (67%) a birth weight of 2500 g or more. Multiple births resulted in 25 children with CP (14%); 25 were twins from 23 pregnancies. Thirteen children (7.3%) were small for gestational age and 11 (6.2%) were large for gestational age. The mean deviation was +0.29 SD; +0.26 SD for boys and +0.3 SD for girls. The mean maternal age was 30.5 years, whereas in the population, the average age was 29.5. This was the first child in 50%, the 2nd child in 29% and the 3rd child or more in 21%. Care in a neonatal unit was given to 122 of the children (69%) who were diagnosed with CP, compared with 12% in the population.

There were five stimulated pregnancies and 13 in-vitro fertilizations, resulting in 18 children with CP (8% compared with 5% in children born 1995–1998). In this group, 12 were born preterm and 11 were the result of twin pregnancies. Ten children had diplegia, three had hemiplegia, another three had dyskinetic CP and two had ataxia.

Gender differences

Of the 177 children, 88 were boys and 89 were girls. The even distribution was due to the female predominance in the term group, where 51 (44%) were boys and 64 were girls. In the preterm group, there was a male predominance, with 37 (60%) boys and 25 girls.


The gestational age-specific prevalence for <28 gestational weeks was 55.6 per 1000 live births (12/216), 43.7 per 1000 for 28–31 weeks (22/503), 6.1 per 1000 for 32–36 weeks (28/4598) and 1.43 per 1000 for >36 weeks (115/80 420). The birth-weight-specific prevalence was 58.3 per 1000 for a birth weight of <1000 g (13/223), 44.0 for a birth weight of 1000–1499 g (16/364), 9.9 per 1000 for a birth weight of 1500–2499 g (30/3064) and 1.44 per 1000 for a birth weight of 2500 g or more (118/82 086). The prevalence by gestational age is shown in Figure 3. For extremely preterm children, the decrease in prevalence was significant (p < 0.05), compared with the previous birth-year cohort of 1995–1998. The increase in the prevalence of CP in children born at term reached significance (p < 0.01).


Figure 3.  Prevalence of CP by gestational age, 1975–2002.

Download figure to PowerPoint

CP types

The prevalence by CP type is shown in Figure 4. Hemiplegia, or unilateral spastic CP, accounted for 38% (68/177), diplegia and tetraplegia for 32% (57/177) and 7% (13/177), respectively. Taken together, diplegia and tetraplegia, or bilateral spastic CP, comprised 39%. Extremely preterm bilateral spastic CP decreased, parallel to the gestational-age prevalence (Fig. 3). Seventeen percent had dyskinetic CP (30/177) and 5% had ataxia (9/177). In the growing group of children born at term, the distribution of CP types was relatively unchanged compared with previous cohorts, with the exception of tetraplegia, or severe bilateral spastic CP, which had increased its percentage from 3% to 8% (0.1 < p < 0.2; ns). The rise in dyskinetic CP since the 1980s had reached significance (p < 0.01).


Figure 4.  Prevalence of CP by CP type, according to Hagberg’s classification, 1975–2002.

Download figure to PowerPoint


Neuroimaging information was available in 169 cases (95%); ultrasound only in 9, CT in 111 and MRI in 86 (CT only in 74, MRI only in 49, CT and MRI in 37). The findings on CT and MRI in 160 children are presented by CP type and gestational age group in Table 2. Maldevelopment was found in 19/160 (12%), 17 of whom were born at term or near term. White-matter lesions were present in 49/160 (31%), 27 of whom were born at term or near term. Cortical/subcortical lesions were found in 45/160 (28%), 32 of whom were born at term or near term. Basal ganglia lesion was the major finding in 18/160 (11%), all born at term or near term. The majority of the latter lesions were considered to be peri-/neonatally derived. A combination of cortical/subcortical and basal ganglia lesions was found in 15 children. Cerebellar findings were present in three children, one of whom had hypoplasia of the cerebellum, whereas two had sustained a cerebellar haemorrhage in the peri-/neonatal period. In hemiplegia, or unilateral spastic CP, white-matter lesions and subcortical lesions were most frequent, comprising 45% and 42%, respectively. In diplegia, white-matter lesions were present in 40% and cortical/subcortical lesions in 24%. Cortical/subcortical and basal ganglia lesions dominated in dyskinetic CP. Neuroimaging in ataxia produced miscellaneous findings and was often normal. Overall, findings were normal in 16%. In 14 of the 26 children with a normal finding, only CT had been performed.

Table 2.   Neuroimaging findings by CP type and gestational age group in 160 children born in 1999–2002
CT/MRI findings by CP typeHemiplegiaDiplegiaTetraplegiaDyskinetic CPAtaxiaTotal (%)
<34 weeks≥34 weeks<34 weeks≥34 weeks<34 weeks≥34 weeks<34 weeks≥34 weeks<34 weeks≥34 weeks
  1. +Additional basal ganglia lesions in eight children with cortical/subcortical lesions dominating.

  2. *Additional parasagittal ± hippocampus lesions, in seven children with basal ganglia lesions dominating.

  3. aCerebellar haemorrhage in the peri/neonatal period.

  4. bSequelae after congenital cerebral PNET (primitive neuroectodermal tumour).

  5. cNormal CT but no MRI performed in one child, normal MRI in one child.

  6. dUltrasound performed, three normal and one with periventricular and plexus haemorrhage.

  7. eUltrasound performed in five, one normal and four with periventricular and plexus haemorrhage, no ultrasound performed in one.

Maldevelopment 7 421 3 219 (12)
White-matter lesions621146  2   49 (31)
Cortical/subcortical lesions114+++111+++16+ 10+ 145 (28)
Basal ganglia/thalamus lesions 2* 2 1 13******  18 (11)
Other abnormalities 1a 1a,1b      3 (2)
Normal findings1746 2c11 426 (16)
Total8521931310327 7160
CT/MRI not performed4d46e1     217


The division into aetiological periods is shown in Table 3. In overall terms, 64 children (36%) were assigned to the prenatal period, all born at term or moderately preterm. The most common neuroimaging finding in this group was periventricular white-matter lesions, present in 42%, followed by the maldevelopment in 23%.

Table 3.   Aetiological periods by gestational age in 177 children with CP born in 1999–2002
Gestational agePretermTermTotal
<28 weeks28–31 weeks32–36 weeks>36 weeks
  1. Items higher on the list took precedence over those lower on the list, with the exception of peri/neonatal intra-cerebral haemorrhage/infarction, neonatal shock and brain oedema (3).

Intra-uterine infection00033
CNS maldevelopment0051015
Intra-cranial haemorrhage/infarction/hydrocephalus0011213
Other prenatal CNS abnormalities00246
For children born at ≥34 weeks of gestation with normal delivery and peri/neonatal period: periventricular atrophy/porencephaly0042327
Intra-cranial haemorrhage/infarction/neonatal shock/brain oedema ± HIE9632543
CNS infection and/or sepsis12216
For children born at ≥34 weeks of gestation: HIE0041721
For children born at <34 weeks of gestation: periventricular atrophy and/or periventricular haemorrhage with normal initial ultrasound10102
For children born at <34 weeks of gestation: low Apgar and/or low pH/mechanical ventilation >7 days or complicated by pneumothorax11002

In 75 (42%), the aetiology was considered to be peri- or neonatal. In the 32 children born preterm, intra-cranial haemorrhage or infarction was the most frequent background, found in 18 (56%). Hypoxic-ischaemic encephalopathy, neonatal shock and/or brain oedema were the most common perinatal aetiology present among 42 of the 43 children born at term.

Children born at term with a considered peri- or neonatal aetiology had cortical/subcortical lesions, as well as basal ganglia lesions. Children born at term or near term with an Apgar score of <5 at 5 min had significantly more basal ganglia lesions than children with an Apgar score of ≥5 at 5 min (15/23 vs 10/105; p < 0.001).

Seventeen of 134 children (13%) born at term or near term fulfilled the ACOG criteria regarding an acute intra-partum hypoxic event severe enough to cause CP, while another five children (two with ataxic diplegia, one with spastic diplegia and two with hemiplegia) had an umbilical cord pH below 7 and neonatal encephalopathy, but did not fulfil the criterion for CP type. Compared with previous cohorts of children with CP born at term or near term, there was a trend, close to significance, towards more children fulfilling the ACOG criteria of intra-partum events severe enough to cause CP (17/134 in the present cohort compared with 7/120 in children born in 1995–1998, p < 0.06;ns).

Thirty-eight children (21%), 20 of whom were born at term, remained unclassified as to aetiological period.

Unclassifiable cases

The unclassifiable cases are presented in Table 4. In 38 children, 20 of whom were born at term, there was insufficient information to assign them to an aetiological period. In the term children, the neuroimaging findings were normal in 17/20 and missing in three.

Table 4.   Unclassifiable cases, risk factors and neuroimaging findings in the birth-year cohort 1999–2002
Risk factor/eventPreterm n = 18Term n = 20Total n = 38
  1. *Infections during pregnancy or labour (5), diabetes mellitus and hypertension (1), essential hypertension (1), Crohn’s disease (1), thrombotic disease (1) and severe motor impairment (1).

  2. Foetal distress (8), severe bleeding (3), severe preeclampsia and/or pathological umbilical artery flow (3) in the preterm group, aberrant presentation (1) and disrupted umbilical cord (1) in the term group.

  3. Seizures (2), infection (1), hypoglycaemia and hypothermia (1, diagnosed with congenital hypothyreosis), hypothermia (1).

  4. §In two preterm children, ultrasound revealed a subependymal haemorrhage.

Apgar at 5 min <5000
Multiple pregnancy527
Maternal disorder4*6*10
Growth deviation
Stimulated pregnancy/in-vitro fertilization628
 Disruption of umbilical cord011
Instrumental delivery
Care in neonatal care unit18523
CT/MRI findings
 White-matter lesions505
 Cortical/subcortical lesions101
 Basal ganglia lesions101
 Normal findings31720
 Not performed8§311

In the children born preterm, instrumental delivery was performed for emergency reasons in 14/18. In five preterm children, periventricular atrophy was present, one had a cortical/subcortical lesion and one had a post-ischaemic basal ganglia lesion. It was, however, unclear whether the lesions occurred in the prenatal or peri/neonatal period.

Post-neonatal cases

Of the nine post-neonatal cases, four had a history of CNS infection, resulting in hemiplegia in three and ataxia in one. Two had a cerebral infarction, resulting in hemiplegia, while two children, one with diplegia and one with hemiplegia, had suffered a traumatic brain injury before the age of two. One had sustained a circulatory collapse due to hypoglycaemia, resulting in tetraplegia.


  1. Top of page
  2. Abstract
  3. Introduction
  4. Method
  5. Results
  6. Discussion
  7. Acknowledgements
  8. References

A significant decrease in CP prevalence since the 1980s up to the birth-year period 1995–1998 has been reported from this long-term study of the panorama of CP in Sweden (3). This is mainly due to the decrease in CP in children born preterm, a finding also recognized in other population-based studies (13). This overall trend has now ceased, due to an apparent rise in CP in children born at term, while CP in children born preterm is still decreasing; now also in the group born before 28 weeks of gestation. More children were the result of stimulated pregnancies or in-vitro fertilization before. However, studies have shown that IVF in itself does not increase the risk of CP in the infant, but it is involved in the increased risk of preterm birth (14,15). The previous male predominance was also absent. A similar, uniform gender distribution has been reported from Iceland (16). In this study, the uniform distribution of gender was due to the female predominance in term-born children. Looking back to the 1970s, no trend regarding gender distribution could be seen. The expected male predominance was, however, still found in preterm children. The increase in dyskinetic CP since the beginning of the 1990s continued. Children born at term now dominate the panorama of CP more than before, and dyskinetic CP is a CP type characteristic of children born at term and with depressed vital signs at birth (17). A recent report from the SCPE network of Europe has also indicated an increasing trend regarding dyskinetic CP in children with normal birth weight (18). The decrease in preterm CP has previously correlated well with a decrease in bilateral spastic CP (4,5). This is no longer the case, as there is now an increase in children with severe bilateral spastic CP, or tetraplegia, born at term. However, there is still a decrease in bilateral spastic CP in children born preterm. The advances in maternal and peri-/neonatal surveillance and care are probably responsible for the latter. The risk factors’ characteristic of children with perinatal adverse events born at term has still not been sufficiently addressed. A well known aetiological factor in dyskinetic CP is HIE in infants born at term or near term. It can be speculated that this factor has not decreased, and that children suffering from HIE may survive to a larger extent than before. The cooling of the head or body after asphyxia shows promising results in reducing morbidity and mortality (19,20), whereas pharmacological treatment is less well developed, despite intensive research into the mechanisms of perinatal brain damage (21,22). Recently, it was suggested that erythropoietin improved the outcome after ischaemia (23). A genetic contribution to the risk of CP has been detected by Gibson et al. in a population-based study (24), whereas infectious or thrombophilic factors, for example, are highlighted by others (25,26). The origins of CP remain only partially explained, although the description and dating of the lesions are increasingly detailed, mainly due to the advances in neuroimaging (27–30). In this study, CT and/or MRI had been performed in 90% of the children. CT was the only imaging modality in 74 children which may be insufficient. In the 14 children with normal finding on CT, an MRI might have revealed lesions explaining the CP. MRI was preferred to CT in the consensus statement about the diagnostic assessment of cerebral palsy by the American Academy of Neurology (31). In this study, CP was considered to be prenatally derived in more than one-third, while in about 40%, indications of a peri-/neonatal origin were found. Slightly fewer children were assigned to the unclassified group, 21% compared to 30% in the previous cohort of children born in 1995–1998. The combination of risk factors to create a causal pathway is still a relevant concept (32) and, in combination with MRI, the plausible time frame of injury may be narrowed.

In conclusion, the total prevalence of CP in western Sweden ceased to decrease and was found to be on a par with other European countries. While the prevalence of CP in children born preterm continued to decrease, the children born at term now dominate more than before, including a typical subgroup of term-born children, namely those with dyskinetic CP.


  1. Top of page
  2. Abstract
  3. Introduction
  4. Method
  5. Results
  6. Discussion
  7. Acknowledgements
  8. References

This study was supported by grants from the Norrbacka-Eugenia Foundation, the AnnMari and Per Ahlqvist Foundation, the Linnea and Josef Carlsson Foundation, the Torbjörn Jebner Memorial Foundation, the Västra Götaland Region and the Folke Bernadotte Foundation. We are indebted to the Medical Birth Registry Office at the Swedish National Board of Health and Welfare for information on vital statistics. We would also like to express our thanks to all our colleagues at the paediatric and habilitation departments in the study area.


  1. Top of page
  2. Abstract
  3. Introduction
  4. Method
  5. Results
  6. Discussion
  7. Acknowledgements
  8. References
  • 1
    Bax M, Goldstein M, Rosenbaum P, Leviton A, Paneth N, Dan B, et al. Proposed definition and classification of cerebral palsy, April 2005. Dev Med Child Neurol 2005; 47: 5716.
  • 2
    Hagberg B, Hagberg G, Olow I. The changing panorama of cerebral palsy in Sweden 1954–1970. I. Analysis of the general changes. Acta Paediatr Scand 1975; 64: 18792.
  • 3
    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: 28794.
  • 4
    Himmelmann K, Beckung E, Hagberg G, Uvebrant P. Bilateral spastic cerebral palsy – prevalence through four decades, motor function and growth. Eur J Paediatr Neurol 2007; 11: 21522.
  • 5
    Hagberg B, Hagberg G, Olow I, V Wendt L. The changing panorama of cerebral palsy in Sweden. VII. Prevalence and origin in the birth year period 1987–90. Acta Paediatr 1996; 85: 95460.
  • 6
    Surveillance of cerebral palsy in Europe: a collaboration of cerebral palsy surveys and registers. Dev Med Child Neurol 2000; 42: 81624.
  • 7
    Uvebrant P. Hemiplegic cerebral palsy. Aetiology and outcome. Acta Paediatr Scand 1988; 345 Suppl: 1100.
  • 8
    Niklasson A, Ericson A, Fryer JG, Karlberg J, Lawrence C, Karlberg P. An update of the Swedish reference standards for weight, length and head circumference at birth for given gestational age (1977–1981). Acta Paediatr Scand 1991; 80: 75662.
  • 9
    Krägeloh-Mann I. Imaging of early brain injury and cortical plasticity. Exp Neurol 2004; 190: 8490.
  • 10
    Papile LA, Burstein J, Burstein R, Koffler H. Incidence of evolution of subependymal and intraventricular hemorrhage; a study of infants with birth weights less than 1,500 g. J Pediatr 1978; 92: 52943.
  • 11
    Krägeloh-Mann I, Hagberg G, Meisner C, Haas G, Eeg-Olofsson KE, Selbmann HK, et al. Bilateral spastic cerebral palsy – a collaborative study between southwestern Germany and western Sweden. III: aetiology. Dev Med Child Neurol 1995; 37: 191203.
  • 12
    ACOG. The American College of Obstetricians and Gynecologists’ Task Force on Neonatal Encephalopathy and Cerebral Palsy, the American College of Obstetricians and Gynecologists, the American Academy of Pediatrics. Neonatal encephalopathy and cerebral palsy: defining the pathogenesis and pathophysiology. Washington, DC: The American College of Obstetricians and Gynecologists, 2003.
  • 13
    Platt MJ, Cans C, Johnson A, Surman G, Topp M, Torrioli MG, et al. Trends in cerebral palsy among infants of very low birthweight (<1500 g) or born prematurely (<32 weeks) in 16 European centres: a database study. Lancet 2007; 6: 369.
  • 14
    Hvidtjørn D, Schieve L, Schendel D, Jacobsson B, Sværke C, Thorsen P. Cerebral palsy, autism spectrum disorders, and developmental delay in children born after assisted conception: a systematic review and meta-analysis. Arch Pediatr Adolesc Med 2009; 163: 7283.
  • 15
    Middelburg KJ, Heineman MJ, Bos AF, Hadders-Algra M. Neuromotor, cognitive, language and behavioural outcome in children born following IVF or ICSI – a systematic review. Hum Reprod Update 2008; 14: 21931.
  • 16
    Sigurdardóttir S, Thórkelsson T, Halldórsdóttir M, Thorarensen O, Vik T. Trends in prevalence and characteristics of cerebral palsy among Icelandic children born 1990 to 2003. Dev Med Child Neurol 2009; 51: 35663.
  • 17
    Andersen GL, Irgens LM, Haagaas I, Skranes JS, Meberg AE, Vik T. Cerebral palsy in Norway: prevalence, subtypes and severity. Eur J Paediatr Neurol 2008; 12: 413.
  • 18
    Himmelmann K, McManus V, Hagberg G, Uvebrant P, Krägeloh-Mann I, Cans C, et al. Dyskinetic cerebral palsy in Europe: trends in prevalence and severity. Arch Dis Child 2009; 94: 9216. Epub 12 May 2009.
  • 19
    Shankaran S, Laptook AR, Ehrenkranz RA, Tyson JE, McDonald SA, Donovan EF, et al. Whole-body hypothermia for neonates with hypoxic-ischemic encephalopathy. N Engl J Med 2005; 353: 157484.
  • 20
    Azzopardi DV, Strohm B, Edwards AD, Dyet L, Halliday HL, Juszczak E, et al. Moderate hypothermia to treat perinatal asphyxial encephalopathy. N Engl J Med 2009; 361: 134958.
  • 21
    Johnston MV, Hoon AH Jr. Possible mechanisms in infants for selective basal ganglia damage from asphyxia, kernicterus, or mitochondrial encephalopathies. J Child Neurol 2000; 15: 58891.
  • 22
    Hagberg H, Mallard C, Rousset CI, Wang X. Apoptotic mechanisms in the immature brain: involvement of mitochondria. J Child Neurol 2009; 24: 11416.
  • 23
    Zhu C, Kang W, Xu F, Cheng X, Zhang Z, Jia L, et al. Erythropoietin improved neurologic outcomes in newborns with hypoxic-ischemic encephalopathy. Pediatrics 2009; 124: e21826.
  • 24
    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: 107985.
  • 25
    Neufeld MD, Frigon C, Graham AS, Mueller BA. Maternal infection and risk of cerebral palsy in term and preterm infants. J Perinatol 2005; 25: 10813.
  • 26
    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: 99107.
  • 27
    Cowan F, Rutherford M, Groenendaal F, Eken P, Mercuri E, Bydder GM, et al. Origin and timing of brain lesions in term infants with neonatal encephalopathy. Lancet 2003; 361: 73642.
  • 28
    Robinson MN, Peake LJ, Ditchfield MR, Reid SM, Lanigan A, Reddihough DS. Magnetic resonance imaging findings in a population-based cohort of children with cerebral palsy. Dev Med Child Neurol 2009; 51: 3945.
  • 29
    Okereafor A, Allsop J, Counsell SJ, Fitzpatrick J, Azzopardi D, Rutherford MA, et al. Patterns of brain injury in neonates exposed to perinatal sentinel events. Pediatrics 2008; 121: 90614.
  • 30
    Logitharajah P, Rutherford MA, Cowan FM. Hypoxic-ischemic encephalopathy in preterm infants: antecedent factors, brain imaging and outcome. Pediatr Res 2009; 66: 2229.
  • 31
    Ashwal S, Russman BS, Blasco PA, Miller G, Sandler A, Shevell M, et al. Quality Standards Subcommittee of the American Academy of Neurology; Practice parameter: diagnostic assessment of the child with cerebral palsy. Neurology 2004; 62: 85163.
  • 32
    Stanley F, Blair E, Alberman E. Cerebral palsies: epidemiology and causal pathways. Clinics in developmental medicine. Vol 151. New York: Cambridge University Press, 2000.