A neurophysiological-metabolic model for burst suppression
A neurophysiological-metabolic model for burst suppression
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DOI：
10.1073/pnas.1121461109
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发表时间：
2012-02-21
影响因子：
11.1
通讯作者：
Brown, Emery N.
中科院分区：
文献类型：
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作者：
Ching, ShiNung;Purdon, Patrick L.;Brown, Emery N.
突发抑制是一种脑电图 (EEG) 模式，其中高压活动与等电静止交替。它是大脑失活的特征，通常在深度全身麻醉、体温过低以及昏迷和早期婴儿脑病等病理状态下观察到。我们提出了一种统一的突发抑制机制，可以考虑所有这些条件。通过构建生物物理计算模型，我们展示了爆发抑制的主要特征是如何通过神经元动力学和大脑代谢之间的相互作用而产生的。该模型表明，在每种情况下，大脑代谢率的降低，加上 ATP 门控钾通道的稳定特性，都会导致特征性的抑制时期。因此，该模型对实验和临床相关性做出了许多具体预测。
Burst suppression is an electroencepholagram (EEG) pattern in which high-voltage activity alternates with isoelectric quiescence. It is characteristic of an inactivated brain and is commonly observed at deep levels of general anesthesia, hypothermia, and in pathological conditions such as coma and early infantile encephalopathy. We propose a unifying mechanism for burst suppression that accounts for all of these conditions. By constructing a biophysical computational model, we show how the prevailing features of burst suppression may arise through the interaction between neuronal dynamics and brain metabolism. In each condition, the model suggests that a decrease in cerebral metabolic rate, coupled with the stabilizing properties of ATP-gated potassium channels, leads to the characteristic epochs of suppression. Consequently, the model makes a number of specific predictions of experimental and clinical relevance.