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Published on: November 20, 2015
Etiology of cerebral palsy
1Department of Paediatrics, Vestfold Hospital Tønsberg, Norway. alf.meberg@siv.no
Insights
Cerebral palsy (CP) affects 2.3 per 1000 infants, with perinatal/neonatal factors being key causes. Identifying these factors, like brain injury in low birthweight infants, may improve CP prevention strategies.
Area of Science:
- Neurology
- Pediatrics
- Public Health
Background:
- Cerebral palsy (CP) is a significant developmental disorder.
- Understanding its prevalence and etiological factors is crucial for prevention and intervention.
Purpose of the Study:
- To determine the prevalence of cerebral palsy (CP) in a defined population.
- To identify the etiological factors contributing to CP, focusing on perinatal/neonatal causes.
Main Methods:
- A population-based study was conducted, registering CP cases in children born between 1970 and 1999.
- Exclusion criteria included cases with postneonatal etiology.
- Data analysis focused on birth weight, etiological classification (prenatal, perinatal/neonatal, unclassifiable), and specific injury types.
Main Results:
- A total of 166 CP cases were registered, yielding a prevalence of 2.3 per 1000 live births.
- Low birthweight infants (LBWIs) accounted for 40% of cases, while normal birthweight infants (NBWIs) comprised 60%.
- Perinatal/neonatal etiology was identified in 47% of cases; intra/periventricular hemorrhages (IVH/PVH), periventricular leukomalacia (PVL), and cerebral infarctions (CI) were common in LBWIs, whereas hypoxic-ischemic encephalopathy (HIE) predominated in NBWIs.
Conclusions:
- Perinatal/neonatal brain injury is a substantial cause of cerebral palsy.
- Specific injury patterns differ between LBWIs (IVH/PVH/PVL/CI) and NBWIs (HIE).
- These findings suggest a greater potential for CP preventability than previously recognized.
Aims:
To register the prevalence of cerebral palsy (CP) and determine etiological factors for the condition.
Methods:
Population based study with registration of CP-cases in children born during the 30-year period 1970-99. Cases with postneonatal etiology were excluded.
Results:
166 CP-cases were registered among 70 824 children, a prevalence of 2.3 per 1000 live born infants. The prevalence did not change significantly during the period. 66 (40%) were low birthweight infants (LBWIs; <2500 g), and 100 (60%) normal birthweight infants (NBWIs; > or = 2500 g). The origin was classified as prenatal in 37 (22%), perinatal/neonatal in 78 (47%) and unclassifiable in 51 (31 %). In LBWIs 39/66 (59%) had a perinatal/neonatal etiology, most frequently intra- or periventricular hemorrhages (IVH/PVH) and/or periventricular leukomalacia (PVL) or cerebral infarctions (CI) (17; 44%). In NBWIs 39/100 (39%) had a perinatal etiology, most frequently hypoxic-ischemic encephalopathy (HIE) (31; 79%).
Conclusions:
In a substantial percentage of CP-cases perinatal/neonatal brain injury was classified as the cause. Among these IVH/PVH/PVL/CI dominated in LBWIs, while HIE dominated in NBWIs. Our data may point to preventability of a larger part of CP than earlier suggested.
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