|
|
|
| MRI analysis of benzene toxic encephalopathy |
| XIE Pinnan1, CHEN Qi2, XU Jingxuan2, WANG Yingying2, TAO Yuanping2, XIE Yibing1, WU Aiqin2, XU Chongyong2 |
1.Department of Radiology, Yongjia People’s Hospital, Wenzhou, 325100; 2.Department of Radiology, the Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325027
|
|
| Cite this article: |
|
XIE Pinnan,CHEN Qi,XU Jingxuan, et al. MRI analysis of benzene toxic encephalopathy[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2018, 48(7): 535-538.
|
|
|
|
Abstract Objective: To study the dynamic MRI characteristics of benzene toxic encephalopathy. Methods: Complete imaging and clinical data of 35 cases with benzene toxic encephalopathy were collected from 4 hospitals of Wenzhou between March 2009 and November 2016. The imaging characteristics of benzene toxic encephalopathy were retrospectively analyzed. Results: All patients had a definite history of benzene exposure, acute or chronic onset. The clinical manifestations included the damage of central nerve system, the decline of routine blood leucocytes, the abnormality of EEG and the rise of cerebrospinal fluid pressure in lumbar puncture, et al. The arc zone of subcortical white matter fiber was invaded in 35 cases of benzene toxic encephalopathy on MRI scan, demonstrating a sign of “kwai petals” or “flame” shape. “Butterfly” change on both dentate nuclei of cerebellum was seen in 33 cases. The number of external capsule and lentiform nucleus was involved in 28 cases and 16 cases. All lesions demonstrated low signal on T1WI, high signal on T2WI, FLAIR and DWI. High or iso-signal on ADC images appeared in 26 cases and low signal in 9 cases. In 3 cases of MRS examination, the peak of Cho and Cr slightly elevated in 1 case, and no abnormality in 2 cases. No obvious changes appeared on MRI contrast enhancement, SWI and MRA. Conclusion: MRI manifestations of benzene toxic encephalopathy have some characteristics. Combined with the history, MRI can reduce the misdiagnosis of the disease and provide reference for clinical diagnosis and treatment.
|
|
Received: 01 November 2017
|
| |
|
|
|
[1] 丁琪, 魏学兰. 苯中毒机制与治疗分析[J]. 中国医药导报, 2006, 3(30): 34-35.
[2] ZAFARULLAH M, LI W Q, SYLVESTER J, et al. Molecular mechanisms of N-acetylcysteine actions[J]. Cell Mol Life Sci, 2003, 60(1): 6-20.
[3] KONDROVA E, STOPKA P, SOUCEK P. Cytochrome P450 destruction by benzene metabolites 1, 4-benzoquinone and 1, 4-hydroquinone and the formation of hydroxyl radicals in minipig liver microsomes[J]. Toxicol In Vitro, 2007, 21(4): 566-575.
[4] 申东晓, 史须, 王应, 等. 硫氧还蛋白对氢醌细胞毒性的抑制[J]. 中国药理学与毒理学杂志, 2003, 17(1): 55-60.
[5] 陈玲, 夏梦, 林达, 等. 急性苯中毒所致化学性肺水肿的高分辨率CT表现[J]. 中华放射学杂志, 2014, 48(7): 599-600.
[6] 陈延帆, 郑汉朋, 吴海, 等. 苯中毒性脑病的CT与MRI表现[J]. 医学影像学杂志, 2015, 25(3): 407-410.
[7] 曾俊杰, 张秀萍, 韩再德, 等. 苯中毒脑病的MR诊断价值初探[J]. 中国临床医学影像杂志, 2012, 23(6): 414-417.
[8] 谢安明, 丁耀军. 一氧化碳中毒性脑病的MRI弥散加权成像表现与预后的关系[J]. 南昌大学学报(医学版), 2014, 54 (9): 46-49.
[9] 施益芬, 郑周懿, 陈晶晶, 等. TOPO IIα启动子调控因子组蛋白甲基化修饰在苯中毒致造血毒性中的作用[J]. 温州医科大学学报, 2015, 45(6): 391-396. |
|
|
|
