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Updated: Jun 14, 2026
A Battery of Motor Tests in a Neonatal Mouse Model of Cerebral Palsy
Published on: November 3, 2016
[Cerebral palsy and perinatal asphyxia (I--diagnosis)]
1Service de gynécologie-obstétrique, hôpital Mère-Enfant, CHU de Nantes, Nantes, France. georges.boog@wanadoo.fr
Insights
Cerebral palsy (CP) is a brain development disorder impacting movement and posture. Identifying its cause, often perinatal asphyxia, is crucial for diagnosis and differentiating it from other neurological conditions.
Area of Science:
- Neurology
- Developmental Pediatrics
- Obstetrics
Context:
- Cerebral palsy (CP) prevalence remains high despite advancements in fetal monitoring and cesarean delivery rates.
- CP involves motor and potentially sensory, cognitive, and behavioral impairments due to early brain disturbances.
- Perinatal asphyxia is a key factor in term newborns, indicated by specific cord blood acidosis and neonatal encephalopathy.
Purpose:
- To elucidate the role of perinatal asphyxia in cerebral palsy development.
- To establish criteria for dating fetal asphyxia during labor and delivery.
- To differentiate CP caused by asphyxia from other neurological disorders using advanced imaging and placental analysis.
Summary:
- CP is linked to non-progressive disturbances in the developing fetal or infant brain.
- Magnetic resonance imaging (MRI) reveals distinct patterns of brain injury corresponding to acute or prolonged asphyxia.
- Placental histology and definitive brain MRI are essential for accurate diagnosis and etiological determination.
Impact:
- Improved diagnostic accuracy for cerebral palsy.
- Enhanced understanding of the pathophysiology of birth-related brain injury.
- Potential for earlier and more precise interventions for affected newborns.
Abstract:
Cerebral palsy (CP) is a group of disorders of the development of movement and posture, causing activity limitations, that are attributed to nonprogressing disturbances that occurred in the developing fetal or infant brain. The motor abnormalies are often accompanied by disturbances of sensation, perception, cognition, behavior and/or by a seizure disorder. The prevalence of CP has not decreased in developed countries over the past 30 years, despite the widespread use of electronic fetal heart rate monitoring and a 5- to 6-fold increase in the cesarean delivery rate. In the term newborn, CP may be attributed to perinatal asphyxia in case of metabolic acidosis in the cord blood (pH<7,00 and base deficit>12 mmol/L), followed by a moderate or severe neonatal encephalopathy within 24 hours and a further neurological impairement characterized by spastic quadriplegia and dyskinesia/dystonia. Dating the time of fetal asphyxia during delivery is possible when there are acute catastrophic complications during labor and unexpected acute or progressive fetal heart rate anomalies after a normal admission test, when there is a need for intensive neonatal resuscitation, a multi-organ failure within 72 hours of birth and visualization of acute non focal cerebral abnormalities, mainly by early magnetic resonance imaging (MRI). MRI sequences show either a brain-damaged pattern of the central basal ganglia, thalami and posterior limbs of internal capsules with relative cortical sparing, in acute, near-total asphyxial insults manifested by a continuous bradycardia or a pattern of cortical injury in the watershed zones and relative sparing of the central grey matter, in prolonged partial asphyxia, manifested by late or atypical variable decelerations with progressive fetal tachycardia, loss of reactivity and absent fluctuation. Prolongation of either type of asphyxial insult results in more global brain damage. In order to differentiate a CP occurring after perinatal asphyxia from other neurological sequelae in relation with infection, hemorrhage, stroke, malformations, genetic or metabolic diseases, it is essential that a definitive information from the brain by MRI and an extensive histological examination of the placenta are at disposal.
