Rogatsky G G, Sonn J, Kamenir Y, Zarchin N, Mayevsky A
Faculty of Life Sciences, Bar-Ilan University, Ramat-Gan, Israel.
J Neurotrauma. 2003 Dec;20(12):1315-25. doi: 10.1089/089771503322686111.
Traumatic brain injury (TBI) is known to be accompanied by an increase in intracranial pressure (ICP) and in some cases, by spontaneous generation of cortical spreading depression (CSD) cycles. However, the role of CSD in the pathophysiology of cerebral contusion is still unknown. A multiparametric monitoring assembly was placed on the right hemisphere of the rat brain to evaluate ICP, DC potential, extracellular K(+), cerebral blood flow (CBF), and electrocorticogram in 27 rats during 5 h. Fluid percussion brain injury (FPBI) with the magnitude of the impact 2.9, 3.3, 4.1, and 5.0 atmospheres was induced to the left parietal cortex in animal groups A, B, C, and D, respectively. A slow increase in ICP was evident, and was pronounced in group C and especially in group D, where four of nine animals died during the monitoring. At the end of the 5 h experiment, the mean ICP levels were 6.75 +/- 2.87, 8.40 +/- 2.70, 12.75 +/- 4.03, 29.56 +/- 9.25, and the mean total number of CSD cycles was 2.00 +/- 1.41, 4.29 +/- 4.23, 11.71 +/- 13.29, and 20.11 +/- 19.26 in groups A, B, C, and D, respectively. The maximal level of intensity of CSD cycle generation after FPBI was obtained in group D, where almost constant activity was maintained until the end of the experiment. A significant coefficient of correlation between ICP level and total number of CSD cycles was found for all ICP measurements (r = 0.47-0.63, p < 0.05, n = 27), however more significant (p < 0.001) was the coefficient during the period of monitoring between 2 and 4 h after FPBI. Our results suggest that numerous repeating CSD cycles are typical phenomena in moderate and especially severe forms of FPBI. The rising number of CSD cycles under condition of an ICP level >/=20 mm Hg may demonstrate, with high probability, the unfavorable development of TBI, caused by growing secondary hypoxic insult.
已知创伤性脑损伤（TBI）会伴有颅内压（ICP）升高，在某些情况下还会伴有皮质扩散性抑制（CSD）周期的自发产生。然而，CSD在脑挫伤病理生理学中的作用仍不清楚。在27只大鼠的大脑右半球放置一个多参数监测装置，持续5小时以评估颅内压、直流电位、细胞外钾离子（K⁺）、脑血流量（CBF）和脑电图。分别对A、B、C和D组动物的左顶叶皮质施加冲击强度为2.9、3.3、4.1和5.0个大气压的流体冲击性脑损伤（FPBI）。颅内压出现缓慢升高，在C组尤其明显，在D组更为显著，监测期间D组9只动物中有4只死亡。在5小时实验结束时，A、B、C和D组的平均颅内压水平分别为6.75±2.87、8.40±2.70、12.75±4.03、29.56±9.25，CSD周期的平均总数分别为2.00±1.41、4.29±4.23、11.71±13.29和20.11±19.26。在D组中，FPBI后CSD周期产生的最大强度水平在实验结束前几乎保持恒定。对所有颅内压测量值而言，发现颅内压水平与CSD周期总数之间存在显著的相关系数（r = 0.47 - 0.63，p < 0.05，n = 27），然而在FPBI后2至4小时的监测期间，该系数更显著（p < 0.001）。我们的结果表明，在中度尤其是重度形式的FPBI中，大量重复的CSD周期是典型现象。在颅内压水平≥20 mmHg的情况下，CSD周期数量的增加很可能表明由于继发性缺氧损伤加剧，TBI的发展不利。
