Proton MR spectroscopy detected glutamate/glutamine is increased in children with traumatic brain injury
Proton MR spectroscopy detected glutamate/glutamine is increased in children with traumatic brain injury
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DOI：
10.1089/0897715042441756
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发表时间：
2004-11-01
影响因子：
4.2
通讯作者：
Kido, D
中科院分区：
文献类型：
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作者：
Ashwal, S;Holshouser, B;Kido, D
创伤性脑损伤（TBI）的成年人已经通过侵入性方法显示出兴奋性神经递质谷氨酸水平增加。目前尚不清楚谷氨酸释放是否有助于原发性或继发性损伤，以及其持续升高是否预示着不良结局。我们机构在成人中的初步研究发现，磁共振波谱（MRS）检测到的谷氨酸/谷氨酰胺（Glx）的早期增加与不良结局相关。因此，我们研究了38名患有TBI的儿童（平均年龄11岁;范围1.6-17岁），在受伤后平均7 +/- 4（范围1-17）天进行定量短回波时间（STEAM，TE = 20 msec）质子MRS，以确定他们的枕叶或顶叶Glx水平是否与损伤的严重程度或结果相关。与对照组相比，TBI儿童的枕叶Glx显著增加（13.5 +/- 2.4 vs. 10.7 +/- 1.8; p = 0.002），但在损伤后6-12个月时，通过儿科脑功能分类量表评分确定，预后良好的儿童与预后不良的儿童之间没有差异。我们也没有发现Glx的量与最初的格拉斯哥昏迷量表评分、昏迷持续时间之间的相关性，也没有发现Glx与光谱代谢物（包括N-乙酰天冬氨酸、胆碱和肌醇）变化之间的相关性。在某种程度上，这可能是因为，在这项研究中，大多数预后不良的患者的研究时间晚于预后良好的患者，可能超过了受伤后Glx峰值升高的时间范围。需要对不同程度损伤的患者进行额外的早期和晚期研究，以评估这种兴奋性神经递质对TBI病理生理学的重要性。
Adults with traumatic brain injury (TBI) have been shown by invasive methods to have increased levels of the excitatory neurotransmitter glutamate. It is unclear whether glutamate release contributes to primary or secondary injury and whether its protracted elevation is predictive of a poor outcome. Preliminary studies at our institution in adults found that early increases in magnetic resonance spectroscopy (MRS)-detected glutamate/glutamine (Glx) were associated with poor outcomes. We therefore studied 38 children (mean age, 11 years; range, 1.6-17 years) who had TBI with quantitative short-echo time (STEAM, TE = 20 msec) proton MRS, a mean of 7 +/- 4 (range, 1-17) days after injury in order to determine if their occipital or parietal Glx levels correlated with the severity of injury or outcome. Occipital Glx was significantly increased in children with TBI compared to controls (13.5 +/- 2.4 vs. 10.7 +/- 1.8; p = 0.002), but there was no difference between children with good compared to poor outcomes as determined by the Pediatric Cerebral Performance Category Scale score at 6-12 months after injury. We also did not find a correlation between the amount of Glx and the initial Glasgow Coma Scale score, duration of coma, nor with changes in spectral metabolites, including N-acetyl aspartate, choline, and myoinositol. In part, this may have occurred because, in this study, most patients with poor outcomes were studied later than patients with good outcomes, potentially beyond the time frame for peak elevation of Glx after injury. Additional early and late studies of patients with varying degrees of injury are required to assess the importance to the pathophysiology of TBI of this excitatory neurotransmitter.