家犬脑挫裂伤^1H—MR波谱研究

^1 H-MR spectroscopy of dog＇s brain contusion and laceration

目的探讨家犬脑挫裂伤MR波谱(MRS)表现及其应用价值。方法家犬10只,200 g砝码1．3 m高以自由坠落方式复制脑挫裂伤动物模型,分6个时间点(1 h、24 h、72 h、5 d、8 d和14 d)行常规MR及MRS检查。各时段检查结束后处死家犬,取挫裂伤处脑组织行病理检查。结果伤后1～24 h,N-乙酰天冬胺酸/肌酸(NAA/Cr)、胆碱类化合物(Cho)/Cr及NAA/Cho下降,NAA/Cr分别为0．843±0．214,0．862±0．204,对侧1．069±0．284,1．048±0．232,t=-7．227,-6．718：Cho/Cr 1．181±0．224,1．243±0．134,对侧1．415±0．305,1．455±0．159,t=-4．332,-4．489：NAA/Cho 0．701±0．147,0．536±0．136,对侧0．832±0．245,0．613±0．165,t=-2．652,-2．665(P值均＜0．05)；病理示挫伤处见局部点状出血、灶性坏死、神经轴突肿胀、小胶质细胞轻度增生。伤后72 h至5 d,NAA/Cr开始升高,Cho/Cr于5 d时为1．517±0．197,高于对侧,对侧为1．387±0．214(t=3．758。P＜0．05)；镜下示炎性细胞浸润明显,血管周围炎、肉芽及纤维瘢痕形成。伤后8～14 d,NAA/Cr与对侧相比差异无统计学意义(0．895±0．105,0．875±0．153,对侧0．989±0．169,0．990±0．173．t= -2．909,-2．471；P值均＞0．05),Cho/Cr高于对侧(1．457±0．168,1．572±0．374,对侧1．334±0．174,1．366±0．352,t=7．312,3．201；P值均＜0．05)；病理示炎性反应及胶质增生更加显著,14 d时肉芽肿形成。各时段均未见异常乳酸峰及脂质峰。结论MRS能无创性检测脑挫裂伤后神经元受损及修复情况,了解其脑组织生化代谢改变,反映损伤的程度,为早期治疗和预后的评价提供理论依据。

Objective To investigate proton magnetic resonance spectroscopy （^1H-MRS） findings and value on dog＇s brain contusion and laceration. Methods Models of focal brain contusion and laceration in 10 dogs were established through hitting on the right frontal-parietal lobe with a freely drop of 200g weight at 1.3 m height. Serial examinations （ 1 h, 24 h, 72 h, 5 day, 8 day and 14 day after trauma） were performed with conventional MRI and ^1H-MRS. NAA/Cr, Cho/Cr and NAA/Cho rates were analyzed with GE system 1.5 T scanner and relative software. After examination, all dogs were executed to death. Pathological study was performed at local brain contusion. Results 1 h and 24 h-post trauma, NAA/Cr, Cho/Cr,NAA/Cho were significantly reduced （ NAA/Cr 0. 843 ± 0. 214,0. 862 ± 0. 204, contralateral ones 1. 069 ±0. 284,1. 048 ±0. 232,t = -7. 227, -6. 718,Cho/Cr 1. 181 ±0. 224,1. 243 ±0. 134,contralateral 1.415±0.305,1.455 ±0.159, t = -4.332, -4.489, NAA/Cho 0.701 ±0.147,0.536 ± 0.136, contralateral 0. 832 ± 0. 245,0. 613 ± 0. 165, t = - 2. 652, - 2. 665. P 〈 0. 05 ）. Microscopy showed focal petechial hemorrhage and necrosis, neuron loss, neuraxonal swelling and small glial cell slightly hyperplasia. Five day post trauma. , Cho/Cr was significantly elevated in comparison with contralateral ones （ 1. 517 ± 0. 197, contralateral 1. 387 ± 0. 214, t = 3. 758. P 〈 0. 05 ）. Pathologically, inflammatory was obvious, peri-angiitis, granula tissue and fibrosis were seen. 8-14 day later, NAA/Cr was not significantly reduced （0. 895 ± 0. 105,0. 875 ± 0. 153, contralateral 0. 989 ± 0. 169,0. 990 ± 0. 173, t = - 2. 909, -2. 471. P 〉 0. 05 ）, Cho/Cr was significantly increased （ 1. 457 ± 0. 168, 1. 572 ± 0. 374, contralaterl 1. 334 ± 0. 174,1. 366 ± 0. 352, t = 7.312,3. 201. P 〈 0. 05 ） Inflammatory and glial hyperplasia was more significant, granuloma were seen. Lipid and Lac peak were not seen at all stages. Conclusion MRS could be a methods to monitor neuron injury and repair, and dynamically to detect the metabolic changes of brain contusion and laceration, reflecting injury severity and provide theory data for early treatment and predicting long-term outcome after trauma.