Kassubek Jan, Juengling Freimut D, Els Thomas, Spreer Joachim, Herpers Martin, Krause Thomas, Moser Ernst, Lücking Carl H
Department of Neurology, University of Freiburg, Breisacher Str. 64, Freiburg, 79106 Germany.
J Neurol Sci. 2003 Aug 15;212(1-2):85-91. doi: 10.1016/s0022-510x(03)00106-0.
Survivors of prolonged cerebral anoxia often remain in the persistent vegetative state (PVS). In this study, long-term PVS patients were investigated by 15O-H(2)O PET to analyze their central processing of pain. The study was approved by the local Ethics Committee, the experiments were performed in accordance with the Helsinki Declaration of 2000. Seven patients remaining in PVS of anoxic origin for a mean of 1.6 years (range 0.25-4 years) were investigated. We performed functional PET of the brain using 15O-labelled water during electrical nociceptive stimulation. Additionally, a brain metabolism study using 18F-fluorodeoxyglucose (FDG) PET and multi-sequence MRI (including a 3-D data set) were acquired in all patients. PET data were analyzed by means of Statistical Parametric Mapping (SPM99) and coregistered to a study-specific brain template. MRI and FDG PET showed severe cortical impairment at the structural and the functional level, that is, general atrophy of various degrees and a widespread significant hypometabolism, respectively. Pain-induced activation (hyperperfusion) was found in the posterior insula/secondary somatosensory cortex (SII), postcentral gyrus/primary somatosensory cortex (SI), and the cingulate cortex contralateral to the stimulus and in the posterior insula ipsilateral to the stimulus (P<0.05, small-volume-corrected). No additional areas of the complex pain-processing matrix were significantly activated. In conclusion, the regional activity found at the cortical level indicates that a residual pain-related cerebral network remains active in long-term PVS patients.
长时间脑缺氧的幸存者常常处于持续性植物状态（PVS）。在本研究中，对长期处于PVS状态的患者进行了(^{15}O-H_{2}O)正电子发射断层扫描（PET），以分析他们对疼痛的中枢处理情况。本研究经当地伦理委员会批准，实验按照2000年《赫尔辛基宣言》进行。研究了7例因缺氧导致处于PVS状态平均1.6年（范围0.25 - 4年）的患者。在电刺激伤害性感受期间，我们使用(^{15}O)标记的水对大脑进行了功能PET检查。此外，所有患者均进行了使用(^{18}F)-氟脱氧葡萄糖（FDG）PET的脑代谢研究以及多序列磁共振成像（MRI，包括三维数据集）。PET数据通过统计参数映射（SPM99）进行分析，并与特定研究的脑模板进行配准。MRI和FDG PET在结构和功能水平上均显示出严重的皮质损伤，即分别为不同程度的普遍萎缩和广泛的显著代谢减低。在岛叶后部/次级躯体感觉皮层（SII）、中央后回/初级躯体感觉皮层（SI）、与刺激对侧的扣带回皮层以及与刺激同侧的岛叶后部发现了疼痛诱发的激活（血流灌注增加）（P<0.05，小体积校正）。复杂疼痛处理矩阵的其他区域未发现明显激活。总之，在皮质水平发现的区域活动表明，长期处于PVS状态的患者中仍有一个残留的与疼痛相关的脑网络处于活跃状态。
