Van Putten H P, Bouwhuis M G, Muizelaar J P, Lyeth B G, Berman R F
Department of Neurological Surgery, Universiteit Utrecht, Utrecht, Netherlands.
J Neurotrauma. 2005 Aug;22(8):857-72. doi: 10.1089/neu.2005.22.857.
Hypoxia and edema are frequent and serious complications of traumatic brain injury (TBI). Therefore, we examined the effects of hypoxia on edema formation after moderate lateral fluid percussion (LFP) injury using NMR diffusion-weighted imaging (DWI). Adult Sprague-Dawley rats were separated into four groups: sham uninjured (S), hypoxia alone (H), trauma alone (T), and trauma and hypoxia (TH). Animals in Groups T and TH received LFP brain injury, with Groups H and TH undergoing 30 min of moderately severe hypoxia (FiO2 = 0.11) immediately after surgery or TBI (respectively). DWIs were obtained at 2, 4, and 24 h and at 1 week post injury, and apparent diffusion coefficient (ADC) maps were constructed. Animals in Groups T and TH showed an early decrease (p < 0.001) in ADC values in the cortex ipsilateral to TBI 4 hr post injury, followed by elevated ADCs 1 week later (p < 0.05). No significant differences in ADC values were seen between T and TH groups in the ipsilateral cortex. In contrast, the ipsilateral hippocampus for Group TH showed only increasing ADC values. This hyperintensity in the ADC map began at 2 h after TBI, was significant by 24 h (p < 0.05), and reached a maximum at 1 week. This hyperintensity was not observed in Group T. Histopathology seen in TBI animals corresponded well with the pathology observed with MRI. Midline shifts reflecting edema were only observed in TBI animals with little difference between normoxic (T) and hypoxic animals (TH). In sum, this study demonstrates that the development and extent of brain edema following TBI can be examined in vivo in rats using DWI technology. TBI resulted in an early decrease in ADC values indicating cytotoxic edema in the cortex that was followed at 1 week by an increase in the ADC that was associated with decreased tissue cellularity. Histopathology corresponded well to the regions of brain injury and edema visualized by T2 and DWI procedures. Overall, the addition of hypoxia to brain injury resulted in a small increase in the magnitude of edema in hippocampus and cortex over that seen with trauma alone.
缺氧和水肿是创伤性脑损伤（TBI）常见且严重的并发症。因此，我们使用核磁共振扩散加权成像（DWI）研究了缺氧对中度侧方流体冲击伤（LFP）后脑水肿形成的影响。将成年Sprague-Dawley大鼠分为四组：假手术未受伤组（S）、单纯缺氧组（H）、单纯创伤组（T）和创伤合并缺氧组（TH）。T组和TH组动物接受LFP脑损伤，H组和TH组分别在手术后或创伤性脑损伤后立即经历30分钟的中度严重缺氧（吸入氧分数 = 0.11）。在损伤后2小时、4小时、24小时和1周时获取DWI图像，并构建表观扩散系数（ADC）图。T组和TH组动物在损伤后4小时，TBI同侧皮质的ADC值早期下降（p < 0.001），随后在1周后ADC值升高（p < 0.05）。在同侧皮质中，T组和TH组之间的ADC值无显著差异。相比之下，TH组同侧海马仅显示ADC值升高。ADC图中的这种高信号在TBI后2小时开始，在24小时时显著（p < 0.05），并在1周时达到最大值。T组未观察到这种高信号。TBI动物的组织病理学与MRI观察到的病理学结果相符。反映水肿的中线移位仅在TBI动物中观察到，常氧（T）和缺氧动物（TH）之间差异不大。总之，本研究表明，使用DWI技术可以在大鼠体内检测TBI后脑水肿的发展和程度。TBI导致ADC值早期下降，表明皮质中存在细胞毒性水肿，随后在1周时ADC值增加，这与组织细胞数量减少有关。组织病理学与通过T2和DWI程序可视化的脑损伤和水肿区域相符。总体而言，脑损伤合并缺氧导致海马和皮质中的水肿程度比单纯创伤时略有增加。
