Zayachkivsky A, Lehmkuhle M J, Ekstrand J J, Dudek F E
Department of Neurosurgery, University of Utah School of Medicine, Salt Lake City, Utah; and.
Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, Utah.
J Neurophysiol. 2015 Nov;114(5):2753-63. doi: 10.1152/jn.00796.2014. Epub 2015 Sep 9.
The relationship among neonatal seizures, abnormalities of the electroencephalogram (EEG), brain injury, and long-term neurological outcome (e.g., epilepsy) remains controversial. The effects of hypoxia alone (Ha) and hypoxia-ischemia (HI) were studied in neonatal rats at postnatal day 7; both models generate EEG seizures during the 2-h hypoxia treatment, but only HI causes an infarct with severe neuronal degeneration. Single-channel, differential recordings of acute EEG seizures and background suppression were recorded with a novel miniature telemetry device during the hypoxia treatment and analyzed quantitatively. The waveforms of electrographic seizures (and their behavioral correlates) appeared virtually identical in both models and were identified as discrete events with high power in the traditional delta (0.1-4 Hz) and/or alpha (8-12 Hz) bands. Although the EEG patterns during seizures were similar in Ha- and HI-treated animals at the beginning of the hypoxic insult, Ha caused a more severe electrographic seizure profile than HI near the end. Analyses of power spectral density and seizure frequency profiles indicated that the electrographic seizures progressively increased during the 2-h Ha treatment, while HI led to a progressive decrease in the seizures with significant suppression of the EEG background. These data show that 1) the hypoxia component of these two models drives the seizures; 2) the seizures during Ha are substantially more robust than those during HI, possibly because ongoing neuronal damage blunts the electrographic activity; and 3) a progressive decrease in background EEG, rather than the presence of electrographic seizures, indicates neuronal degeneration during perinatal HI.
新生儿惊厥、脑电图(EEG)异常、脑损伤和长期神经学转归(如癫痫)之间的关系仍存在争议。在出生后第7天的新生大鼠中研究了单纯缺氧(Ha)和缺氧缺血(HI)的影响;在2小时的缺氧治疗期间,两种模型均会引发EEG惊厥,但只有HI会导致梗死并伴有严重的神经元变性。在缺氧治疗期间,使用新型微型遥测设备记录急性EEG惊厥和背景抑制的单通道差分记录,并进行定量分析。在两种模型中,电图惊厥的波形(及其行为关联)几乎相同,并且在传统的δ(0.1 - 4Hz)和/或α(8 - 12Hz)频段中被识别为具有高功率的离散事件。尽管在缺氧损伤开始时,Ha处理组和HI处理组动物的惊厥期间EEG模式相似,但在接近缺氧结束时,Ha导致的电图惊厥特征比HI更严重。功率谱密度和惊厥频率分布分析表明,在2小时的Ha处理期间,电图惊厥逐渐增加,而HI导致惊厥逐渐减少,EEG背景受到显著抑制。这些数据表明:1)这两种模型中的缺氧成分驱动惊厥;2)Ha期间的惊厥比HI期间的惊厥明显更强烈,可能是因为持续的神经元损伤使电图活动减弱;3)围产期HI期间,背景EEG的逐渐降低而非电图惊厥的出现表明神经元变性。