Related Experiment Videos
[Epileptic signs of neonatal hypoxia-ischemia]
1Sección de Neuropediatría, HIU Virgen del Rocío, Sevilla, España. mrufoc@meditex.es
Insights
Neonatal hypoxic-ischemic (H-I) lesions are the primary cause of epileptic seizures in newborns, often leading to severe neurological deficits and high mortality. While anti-epileptic drugs can control seizures, long-term outcomes remain poor for many infants.
Area of Science:
- Neonatology
- Neurology
- Pediatrics
Context:
- Neonatal convulsions are frequently symptomatic, primarily linked to hypoxic-ischemic (H-I) brain injury.
- The high incidence and severe sequelae of these crises necessitate further investigation.
Purpose:
- To retrospectively analyze histories of neonatal H-I and epileptic crises.
- To evaluate diagnostic concordance and identify key clinical variables.
Summary:
- A study of 54 neonates with H-I and epileptic crises revealed meconium, infection, and hemorrhage as common prenatal factors.
- Birth complications and low Apgar scores were prevalent; subtle seizures were common, with cerebral echography proving most useful diagnostically.
- While anti-epileptic drugs controlled seizures, long-term follow-up showed high mortality (13/54) and significant neurological impairments in survivors.
Impact:
- Neonatal H-I is a major cause of neonatal epileptic crises, associated with substantial mortality and severe neurological sequelae.
- Classical anti-epileptic drugs effectively manage seizures, with Apgar scores and gestational/placental changes serving as important prognostic markers.
- Normal EEGs during seizures may indicate non-epileptic events, especially when accompanied by a positive therapeutic response.
Introduction:
Neonatal convulsions are usually symptomatic and originate mainly from a hypoxic-ischemic (H-I) lesion. The high incidence of crises and their serious sequelas have led us to carry out this retrospective study.
Patients And Methods:
We studied 54 histories of neonatal H-I and epileptic crises, analyzing 45 variables and evaluating their diagnostic concordance.
Results:
In 20 children meconium was detected during gestation and, to a lesser extent, infection and hemorrhage. Birth was dystonic on 48 occasions, 37 at term and 12 preterm. In most cases (27) birth weight was in accordance with gestational age. Apgar scores were always less than 5. The crises, occasional or daily in most cases, were of subtle semiology in 29 children, followed by generalized tonic (23), focal clonic (13), general clonic (11), multifocal clonic (7), focal tonic and multifocal myoclonic (6), focal myoclonic (4) and generalized myoclonic (2) crises. Only 7 EEGs were done during crises (1 normal, 3 with anomalies and 3 with slow basal activity). Paroxystic anomalies were only found on 10 EEGs done between crises. Cerebral echography was the method most used and most useful. Very frequently changes were observed in other organs as the expression of a multisystemic disorder. Most children had abnormalities on neurological examination. In most cases, classical anti-epileptic drugs were used intravenously, and new generation drugs were given if the crises persisted. After an average of 16-19 months of follow-up, 13 children had died and 34 no longer had crises. However, only 20 of the surviving children were considered to be normal, 14 had severe mental retardation, 6 moderate and one slight retardation.
Conclusions:
Neonatal H-I is the main cause of epileptic crises in the RN period, with a high percentage mortality and severe neurological sequelas. The crises are usually well-controlled by classical anti-epileptic drugs, and are an excellent marker, together with the Apgar score and gestational and placental changes. The appearance of normal EEGs during periods of crises should make us doubt the authenticity of subtle crises, perhaps corroborated by a good therapeutic response.