Cerebral hyperglycolysis following severe traumatic brain injury in humans: A positron emission tomography study
Cerebral hyperglycolysis following severe traumatic brain injury in humans: A positron emission tomography study
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DOI：
10.3171/jns.1997.86.2.0241
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发表时间：
1997-02-01
影响因子：
4.1
通讯作者：
Becker, DP
中科院分区：
文献类型：
--
作者：
Bergsneider, M;Hovda, DA;Becker, DP
实验性创伤性脑损伤研究表明，脑高糖酵解是损伤诱导的离子级联反应和神经化学级联反应的病理生理反应。这一发现对细胞活力、对继发性损伤的脆弱性和受影响区域的功能能力具有重要意义。在这项研究之前，没有在人类中检测到创伤后高糖酵解。采用[F-18]氟脱氧葡萄糖正电子发射断层扫描（FDG-PET）对28例重型颅脑损伤患者的脑高糖酶解特点及发生率进行了分析。采用标准脑室模型计算局部脑葡萄糖代谢率（CMRG）。在28例患者中的6例中，通过同时测量动静脉氧和脑血流量（氙-133）的差异来确定总体脑氧代谢率（CMRO(2)）。高糖酶解，定义为葡萄糖利用率的增加，测量高于预期水平两个标准差，在所有6例患者中，FDG-PET和CMRO(2)检测均在损伤后8天内进行，均有记录。另外5例患者在局灶性肿块病灶附近发现局部高糖酵解。在损伤后的第一周内，56%的研究患者推定有高糖酵解的证据。本研究结果表明，创伤性脑损伤的代谢状态应根据葡萄糖代谢和氧代谢来区分。FDG-PET的使用表明，在人类严重头部损伤后，高糖酵解发生在局部和全局。这项临床研究的结果直接补充了先前在脑损伤实验研究中报道的结果，表明成像能力是脑损伤细胞病理生理特征的基本组成部分。
Experimental traumatic brain injury studies have shown that cerebral hyperglycolysis is a pathophysiological response to injury-induced ionic and neurochemical cascades. This finding has important implications regarding cellular viability, vulnerability to secondary insults, and the functional capability of affected regions. Prior to this study, posttraumatic hyperglycolysis had not been detected in humans.The characteristics and incidence of cerebral hyperglycolysis were determined in 28 severely head injured patients using [F-18]fluorodeoxyglucose-positron emission tomography (FDG-PET). The local cerebral metabolic rate of glucose (CMRG) was calculated using a standard compartmental model. In six of the 28 patients, the global cerebral metabolic rate of oxygen (CMRO(2)) was determined by the simultaneous measurements of arteriovenous differences of oxygen and cerebral blood flow (xenon-133). Hyperglycolysis, defined as an increase in glucose utilization that measures two standard deviations above expected levels, was documented in all six patients in whom both FDG-PET and CMRO(2) determinations were made within 8 days of injury. Five additional patients were found to have localized areas of hyperglycolysis adjacent to focal mass lesions. Within the Ist week following the injury, 56% of patients studied had presumptive evidence of hyperglycolysis.The results of this study indicate that the metabolic state of the traumatically injured brain should be defined differentially in terms of glucose and oxygen metabolism. The use of FDG-PET demonstrates that hyperglycolysis occurs both regionally and globally following severe head injury in humans. The results of this clinical study directly complement those previously reported in experimental brain-injury studies, indicating the capability of imaging a fundamental component of cellular pathophysiology characteristic of head injury.