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首页> 外文期刊>Journal of Neurophysiology >Callosal dysfunction explains injury sequelae in a computational network model of axonal injury
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Callosal dysfunction explains injury sequelae in a computational network model of axonal injury

机译：骨os功能障碍解释了轴突损伤的计算机网络模型中的损伤后遗症

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Mild traumatic brain injury (mTBI) often results in neurobehavioral aberrations such as impaired attention and increased reaction time. Diffusion imaging and postmortem analysis studies suggest that mTBI primarily affects myelinated axons in white matter tracts. In particular, corpus callosum, mediating interhemispheric information exchange, has been shown to be affected in mTBI. Yet little is known about the mechanisms linking the injury of myelinated callosal axons to the neurobehavioral sequelae of mTBI. To address this issue, we devised and studied a large, biologically plausible neuronal network model of cortical tissue. Importantly, the model architecture incorporated intra-and interhemispheric organization, including myelinated callosal axons and distance-dependent axonal conduction delays. In the resting state, the intact model network exhibited several salient features, including alpha-band (8-12 Hz) collective activity with low-frequency irregular spiking of individual neurons. The network model of callosal injury captured several clinical observations, including 1) “slowing down” of the network rhythms, manifested as an increased resting-state theta-to-alpha power ratio, 2) reduced response to attentionlike network stimulation, manifested as a reduced spectral power of collective activity, and 3) increased population response time in response to stimulation. Importantly, these changes were positively correlated with injury severity, supporting proposals to use neurobehavioral indices as biomarkers for determining the severity of injury. Our modeling effort helps to understand the role played by the injury of callosal myelinated axons in defining the neurobehavioral sequelae of mTBI.
机译：轻度脑外伤（mTBI）通常会导致神经行为异常，例如注意力减弱和反应时间增加。扩散成像和事后分析研究表明，mTBI主要影响白质区的髓鞘轴突。特别地，已证明介导半球之间信息交换的call体在mTBI中受到影响。关于将髓质a轴突的损伤与mTBI的神经行为后遗症联系起来的机制还知之甚少。为了解决这个问题，我们设计并研究了皮质组织的大型，生物学上合理的神经元网络模型。重要的是，该模型体系结构整合了半球内和半球内组织，包括有髓的call轴突和距离相关的轴突传导延迟。在静止状态下，完整的模型网络表现出几个显着特征，包括具有单个神经元的低频不规则尖峰的alpha波段（8-12 Hz）集体活动。骨call损伤的网络模型捕获了一些临床观察结果，包括1）网络节奏的“减慢”，表现为静息状态theta-α功率比增加; 2）对注意力样网络刺激的反应减少，表现为降低集体活动的频谱能力，以及3）响应刺激而增加种群响应时间。重要的是，这些变化与损伤严重程度呈正相关，支持使用神经行为指标作为确定损伤严重程度的生物标志物的提议。我们的建模工作有助于理解call骨髓鞘轴突损伤在定义mTBI的神经行为后遗症中所起的作用。

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