Video Experimental Relacionado
Updated: Jul 20, 2026
06:24
Mouse Models of Periventricular Leukomalacia
Published on: May 18, 2010
El origen y el momento de las lesiones cerebrales en bebés a término con encefalopatía neonatal
Frances Cowan1, Mary Rutherford, Floris Groenendaal
1Department of Paediatrics, Faculty of Medicine, Imperial College, Hammersmith Hospital, London, UK. f.cowan@imperial.ac.uk
Lancet (London, England)
|March 7, 2003
Resumen
La lesión cerebral neonatal es causada principalmente por eventos durante el nacimiento, no por factores prenatales. Este estudio encontró insultos agudos en la mayoría de los bebés con encefalopatía neonatal o convulsiones, lo que sugiere que los eventos perinatales inmediatos son los más críticos.
Área de la Ciencia:
- Neurología neonatal neurología neonatal.
- La medicina perinatal es una medicina para el perinatal.
- La neurociencia es la neurociencia.
Sus antecedentes:
- La causa de la encefalopatía neonatal y las convulsiones en los bebés a término sigue sin estar clara, con factores prenatales a menudo implicados.
- Falta evidencia de daño cerebral prenatal, lo que lleva a la investigación de los primeros insultos prenatales como una causa.
Objetivo del estudio:
- Para probar la hipótesis de que la encefalopatía neonatal y / o las convulsiones son el resultado de los insultos prenatales tempranos.
- Para distinguir entre las lesiones cerebrales adquiridas antes del parto frente a las adquiridas durante el período intraparto y postparto temprano.
Principales métodos:
- Se realizó una resonancia magnética cerebral o un examen post-mortem en 351 bebés a término con encefalopatía neonatal o convulsiones.
- Los bebés se clasificaron en dos grupos: aquellos con encefalopatía neonatal y evidencia de asfixia perinatal, y aquellos que presentaron convulsiones dentro de los 3 días posteriores al nacimiento sin otros signos de encefalopatía.
- Se excluyeron los bebés con malformaciones congénitas importantes o trastornos cromosómicos.
Principales resultados:
- En los bebés con encefalopatía neonatal y asfixia perinatal (grupo 1), el 80% mostró evidencia de insulto agudo sin lesiones establecidas.
- La lesión prenatal establecida fue rara (<1% en la resonancia magnética, 3/21 en la post mortem).
- En los bebés que presentaban convulsiones (grupo 2), el 69% tenía daño focal agudo, y solo 2 (3%) mostraban evidencia de lesión prenatal.
Conclusiones:
- Los hallazgos sugieren fuertemente que los eventos en el período perinatal inmediato son la causa principal de la lesión cerebral neonatal.
- Si bien los factores prenatales o genéticos pueden predisponer a algunos bebés, los eventos perinatales son los más significativos.
- Esta investigación pone de relieve la importancia del período intraparto en la patogénesis de la lesión cerebral neonatal.
Más Videos Relacionados
07:36Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
Published on: November 20, 2015
09:39Establishing Mouse Models for Zika Virus-induced Neurological Disorders Using Intracerebral Injection Strategies: Embryonic, Neonatal, and Adult
Published on: April 26, 2018
Videos de Conceptos Relacionados
01:07Teratogenicity
The ability of a drug to produce structural deformations and functional abnormalities in the developing embryo or the fetus is called teratogenicity, and the drug producing this effect is known as a teratogen. Teratogenic effects include stillbirth, miscarriage, intrauterine growth restriction, and neurocognitive delay. A teratogen may affect the embryo at different stages of development, which is important in determining the type and extent of the damage. During blastocyst formation, the early...
01:29Biological Causes of Schizophrenia
Schizophrenia, a severe psychiatric disorder, arises from a complex interplay of biological factors, including genetic predisposition, structural brain abnormalities, neurotransmitter dysregulation, and developmental irregularities. These factors collectively contribute to the onset and progression of the disorder, which typically manifests in late adolescence or early adulthood.
Genetic Factors in Schizophrenia
The genetic basis of schizophrenia is strongly supported by family and twin studies.
Genetic Factors in Schizophrenia
The genetic basis of schizophrenia is strongly supported by family and twin studies.
01:28Development of the Oral Microbiota
The establishment of the oral microbiome begins before birth, challenging the long-held belief that the fetal oral cavity is sterile. The presence of oral microbes such as Streptococcus and Fusobacterium in amniotic fluid suggests that microbial exposure may occur in utero, potentially through translocation from the maternal oral or gastrointestinal tract. This early colonization primes the neonatal immune system and sets the stage for subsequent microbial succession. Maternal health,...
01:19Encephalitis l: Introduction
Encephalitis is inflammation of the brain parenchyma, most often due to infections or autoimmune processes. It presents with neuropsychiatric features such as fever, altered mental status, behavioral changes, cognitive dysfunction, seizures, focal deficits, and sometimes autonomic instability. In some cases, the meninges are also involved, resulting in meningoencephalitis.Infectious CausesInfectious encephalitis is most commonly viral but can also result from bacterial, fungal, or parasitic...
01:26Encephalitis ll: Pathophysiology
Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
01:26Brain Abscess l: Introduction
A brain abscess is a focal, intracerebral infection characterized by a localized collection of pus within the brain parenchyma, resulting from microbial invasion and the body’s inflammatory response. It progresses through stages: early and late cerebritis, followed by early and late capsule formation, reflecting tissue destruction, immune response, and eventual encapsulation.Etiology and PathogenesisCausative organisms vary with source and host factors, often involving polymicrobial infections,...