Zanelli S, Goodkin H P, Kowalski S, Kapur J
Department of Pediatrics, University of Virginia, Charlottesville, VA, USA.
Department of Pediatrics, University of Virginia, Charlottesville, VA, USA; Department of Neurology, University of Virginia, Charlottesville, VA, USA.
Neurobiol Dis. 2014 Aug;68:37-46. doi: 10.1016/j.nbd.2014.03.005. Epub 2014 Mar 15.
Hypoxemic events are common in sick preterm and term infants and represent the most common cause of seizures in the newborn period. Neonatal seizures often lack clinical correlates and are only recognized by electroencephalogram (EEG). The mechanisms leading from a hypoxic/ischemic insult to acute seizures in neonates remain poorly understood. Further, the effects of hypoxia on EEG at various developmental stages have not been fully characterized in neonatal animals, in part due to technical challenges. We evaluated the impact of hypoxia on neonatal mouse EEG to define periods of increased susceptibility to seizures during postnatal development. Hippocampal and cortical electrodes were implanted stereotaxically in C57BL/6 mice from postnatal age 3 (P3) to P15. Following recovery, EEG recordings were obtained during baseline, acute hypoxia (4% FiO2 for 4min) and reoxygenation. In baseline recordings, maturation of EEG was characterized by the appearance of a more continuous background pattern that replaced alternating high and low amplitude activity. Clinical seizures during hypoxia were observed more frequently in younger animals (100% P3-4, 87.5% P5-6, 93% P7-8, 83% P9-10, 33% P11-12, 17% P15, r(2)=0.81) and also occurred at higher FiO2 in younger animals (11.2±1.1% P3-P6 vs. 8.9±0.8% P7-12, p<0.05). Background attenuation followed the initial hypoxemic seizure; progressive return to baseline during reoxygenation was observed in survivors. Electrographic seizures without clinical manifestations were observed during reoxygenation, again more commonly in younger animals (83% P3-4, 86% P5-6, 75% P7-8, 71% P9-10, 20% P11-12, r(2)=0.82). All P15 animals died with this duration and degree of hypoxia. Post-ictal abnormalities included burst attenuation and post-anoxic myoclonus and were more commonly seen in older animals. In summary, neonatal mice exposed to brief and severe hypoxia followed by rapid reoxygenation reliably develop seizures and the response to hypoxia varies with postnatal age and maturation.
低氧血症事件在患病的早产儿和足月儿中很常见,是新生儿期癫痫发作的最常见原因。新生儿癫痫发作通常缺乏临床相关性,只能通过脑电图(EEG)来识别。从缺氧/缺血性损伤到新生儿急性癫痫发作的机制仍知之甚少。此外,缺氧对不同发育阶段新生儿脑电图的影响在新生动物中尚未得到充分表征,部分原因是技术挑战。我们评估了缺氧对新生小鼠脑电图的影响,以确定出生后发育过程中癫痫发作易感性增加的时期。从出生后第3天(P3)到P15,将海马和皮质电极立体定向植入C57BL/6小鼠体内。恢复后,在基线、急性缺氧(4% 氧浓度,持续4分钟)和复氧期间进行脑电图记录。在基线记录中,脑电图的成熟表现为出现更连续的背景模式,取代了高低幅交替活动。在较年幼的动物中,缺氧期间临床癫痫发作更为常见(P3 - 4为100%,P5 - 6为87.5%,P7 - 8为93%,P9 - 10为83%,P11 - 12为33%,P15为17%,r(2)=0.81),并且在较年幼的动物中,在更高的氧浓度下也会发生癫痫发作(P3 - P6为11.2±1.1%,P7 - 12为8.9±0.8%,p<0.05)。背景衰减发生在最初的低氧血症性癫痫发作之后;在复氧期间,存活的动物逐渐恢复到基线水平。在复氧期间观察到无临床表现的心电图形癫痫发作,同样在较年幼的动物中更常见(P3 - 4为83%,P5 - 6为86%,P7 - 8为75%,P9 - 10为71%,P11 - 12为20%,r(2)=0.82)。所有P15动物在这种缺氧持续时间和程度下死亡。发作后的异常包括爆发性衰减和缺氧后肌阵挛,在较年长的动物中更常见。总之,暴露于短暂严重缺氧后快速复氧的新生小鼠可靠地发生癫痫发作,并且对缺氧的反应随出生后年龄和成熟度而变化。