Blacklock J B, Oldfield E H, Di Chiro G, Tran D, Theodore W, Wright D C, Larson S M
J Neurosurg. 1987 Jul;67(1):71-5. doi: 10.3171/jns.1987.67.1.0071.
Glucose utilization by normal and neoplastic cerebral tissue can be measured in humans using positron emission tomography (PET) with fluorine-18-labeled 2-deoxy-D-glucose (FDG). Malignant gliomas are known to exhibit hypermetabolic glucose consumption compared to normal brain. Barbiturate-sensitive cerebral glucose utilization is coupled to neuronal activity, and lesions lacking neuronal activity should be relatively insensitive to barbiturate suppression of glucose utilization. In a study to examine this phenomenon, three patients with cerebral gliomas underwent FDG-PET while awake and during deep barbiturate coma. Cerebral glucose utilization was measured in normal brain, tumor, and a homologous, non-neoplastic control site in the contralateral hemisphere. A glucose utilization ratio for tumor/control tissue was calculated. The mean reduction of glucose utilization during barbiturate coma was: gray matter 67%, white matter 47%, basal ganglia 66%, thalamus 57%, cerebellar cortex 55%, tumor 32%, and the contralateral control site 64%. The mean tumor glucose utilization ratio was 1.48:1 in the awake state and 2.69:1 during barbiturate coma. The changes in gray matter, basal ganglia, thalamus, cerebellar cortex, and tumor/control tissue ratio were significant (p less than 0.05). In one patient, deep tumor invasion not evident on computerized tomography, magnetic resonance imaging, or baseline FDG-PET was apparent during barbiturate-enhanced FDG-PET scanning. The study findings suggest that gliomas resist suppression of glucose utilization by barbiturates; this supports the hypothesis that barbiturates reduce neuronal metabolism by blocking synaptic activity. This differential effect on normal brain and gliomas enhances the capability to assess the extent of neoplastic tissue in brain and may represent the basis for novel therapeutic strategies.
利用正电子发射断层扫描（PET）和氟 - 18标记的2 - 脱氧 - D - 葡萄糖（FDG），可以在人体中测量正常脑组织和肿瘤脑组织对葡萄糖的利用情况。已知恶性胶质瘤与正常脑组织相比，表现出葡萄糖高代谢。巴比妥类药物敏感的脑葡萄糖利用与神经元活动相关，缺乏神经元活动的病变对巴比妥类药物抑制葡萄糖利用应相对不敏感。在一项研究此现象的实验中，三名脑胶质瘤患者在清醒状态和深度巴比妥类药物昏迷期间接受了FDG - PET检查。测量了正常脑、肿瘤以及对侧半球同源的非肿瘤对照部位的脑葡萄糖利用情况。计算了肿瘤/对照组织的葡萄糖利用比率。巴比妥类药物昏迷期间葡萄糖利用的平均降低幅度为：灰质67%，白质47%，基底神经节66%，丘脑57%，小脑皮质55%，肿瘤32%，对侧对照部位64%。清醒状态下肿瘤的平均葡萄糖利用比率为1.48:1，巴比妥类药物昏迷期间为2.69:1。灰质、基底神经节、丘脑、小脑皮质以及肿瘤/对照组织比率的变化具有显著性（p小于0.05）。在一名患者中，计算机断层扫描、磁共振成像或基线FDG - PET上未显示的深部肿瘤浸润在巴比妥类药物增强的FDG - PET扫描中变得明显。研究结果表明，胶质瘤对巴比妥类药物抑制葡萄糖利用具有抵抗性；这支持了巴比妥类药物通过阻断突触活动来降低神经元代谢的假说。这种对正常脑和胶质瘤的不同作用增强了评估脑肿瘤组织范围的能力，可能代表了新治疗策略的基础。
