Marret S, Lardennois C, Mercier A, Radi S, Michel C, Vanhulle C, Charollais A, Gressens P
Department of Neonatal Medicine, Clinique de Pédiatrie et de Puériculture, Hôpital Charles Nicolle, Rouen, France.
Biol Neonate. 2001;79(3-4):236-40. doi: 10.1159/000047098.
Focal arterial infarction in the full-term newborn is an important cause of acquired cerebral lesions in the perinatal period. Clinical motor seizures, most often unifocal, are the nearly constant disclosing symptom confirmed by focal EEG abnormalities. A multifactorial physiopathology is usual, including genetic and perinatal environmental factors. In the past decade, various acquired or genetic thrombophilias have been discussed as risk factors. For several of the involved mechanisms, the excitotoxic cascade could represent a common final pathway leading to neuronal cell death. Early magnetic resonance imaging studies and EEG help to identify the newborns with strokes who are likely to develop hemiplegia and disabilities at school. Protection of the human fetal brain remains difficult, since the triggering factor initiating the excitotoxic cascade is rarely observed. Treatment of seizures is nevertheless necessary, because it seems that they accelerate anoxia-induced neuronal death in animal models of focal hypoxic ischemia.
足月儿局灶性动脉梗死是围生期获得性脑损伤的重要原因。临床运动性癫痫发作，大多为单灶性，是由局灶性脑电图异常证实的几乎恒定的显露症状。通常存在多因素生理病理学，包括遗传和围生期环境因素。在过去十年中，各种获得性或遗传性血栓形成倾向已被讨论为危险因素。对于一些涉及的机制，兴奋性毒性级联反应可能是导致神经元细胞死亡的共同最终途径。早期磁共振成像研究和脑电图有助于识别可能在学校出现偏瘫和残疾的中风新生儿。由于引发兴奋性毒性级联反应的触发因素很少被观察到，保护人类胎儿大脑仍然很困难。然而，癫痫发作的治疗是必要的，因为在局灶性缺氧缺血动物模型中，癫痫发作似乎会加速缺氧诱导的神经元死亡。
