Loma Linda University, Department of Psychology.
University of California, Los Angeles, Department of Neurosurgery.
J Neurosci Res. 2018 Apr;96(4):696-701. doi: 10.1002/jnr.24097. Epub 2017 Jun 13.
Traumatic brain injury (TBI) is associated with acute cerebral metabolic crisis (ACMC). ACMC-related atrophy appears to be prominent in frontal and temporal lobes following moderate-to-severe TBI. This atrophy is correlated with poorer cognitive outcomes in TBI. The current study investigated ability of acute glucose and lactate metabolism to predict long-term recovery of frontal-temporal cognitive function in participants with moderate-to-severe TBI. Cerebral metabolic rate of glucose and lactate were measured by the Kety-Schmidt method on days 0-7 post-injury. Indices of frontal-temporal cognitive processing were calculated for six months post-injury; 12 months post-injury; and recovery (the difference between the six- and 12-month scores). Glucose and lactate metabolism were included in separate regression models, as they were highly intercorrelated. Also, glucose and lactate values were centered and averaged and included in a final regression model. Models for the prediction frontal-temporal cognition at six and 12 months post-injury were not significant. However, average glucose and lactate metabolism predicted recovery of frontal-temporal cognition, accounting for 23% and 22% of the variance, respectively. Also, maximum glucose metabolism, but not maximum lactate metabolism, was an inverse predictor in the recovery of frontal-temporal cognition, accounting for 23% of the variance. Finally, the average of glucose and lactate metabolism predicted frontal-temporal cognitive recovery, accounting for 22% of the variance. These data indicate that acute glucose and lactate metabolism both support cognitive recovery from TBI. Also, our data suggest that control of endogenous fuels and/or supplementation with exogenous fuels may have therapeutic potential for cognitive recovery from TBI.
创伤性脑损伤 (TBI) 与急性脑代谢危机 (ACMC) 有关。中度至重度 TBI 后，ACMC 相关的萎缩似乎在额叶和颞叶中更为明显。这种萎缩与 TBI 后的认知功能恢复较差有关。本研究调查了急性葡萄糖和乳酸代谢在中度至重度 TBI 患者中预测额叶-颞叶认知功能长期恢复的能力。在损伤后 0-7 天通过 Kety-Schmidt 方法测量脑葡萄糖和乳酸代谢率。在损伤后 6 个月、12 个月和恢复期间（6 个月和 12 个月评分之间的差异）计算额叶-颞叶认知处理指数。葡萄糖和乳酸代谢分别包含在单独的回归模型中，因为它们高度相关。此外，葡萄糖和乳酸值被中心化和平均化，并包含在最终的回归模型中。预测 6 个月和 12 个月后额叶-颞叶认知的模型并不显著。然而，平均葡萄糖和乳酸代谢预测了额叶-颞叶认知的恢复，分别解释了 23%和 22%的方差。此外，最大葡萄糖代谢，而不是最大乳酸代谢，是额叶-颞叶认知恢复的逆预测因子，解释了 23%的方差。最后，葡萄糖和乳酸代谢的平均值预测了额叶-颞叶认知的恢复，解释了 22%的方差。这些数据表明，急性葡萄糖和乳酸代谢都支持 TBI 的认知恢复。此外，我们的数据表明，控制内源性燃料和/或补充外源性燃料可能对 TBI 的认知恢复具有治疗潜力。
