常规MRI和^1H—MRS在职业性锰暴露致中枢神经损害中的应用价值

Application of routine MRI and 1H-MRS in evaluating the central neurological damages caused by occupational manganese exposure

目的 探讨MRI和^1H-MRS在诊断职业锰暴露致中枢神经系统损伤中的应用价值.方法 选择18例无症状锰暴露工人（锰暴露组）、12例慢性轻度锰中毒工人（锰中毒组）和19名健康工人（对照组）进行常规MRI和1H-MRS检查,并测定所有受试者血锰含量.在脑组织轴面T1WI上,选择信号最亮区域（尽最选取信号均匀区域）,分别测量苍白球和同侧额叶白质的信号强度,计算出苍白球指数（PI）.^1H-MRS数据进行后处理,计算出代谢产物N-乙酰天冬氨酸（NAA）、胆碱（Cho）、肌醇（ml）与肌酸（Cr）的峰高,并以Cr峰的峰高为标准,测量NAA/Cr、Cho/Cr、mI/Cr比值.采用单因素方差分析分别对3组间PI值、NAA/Cr、Cho/Cr、mI/Cr值及血锰进行比较,锰暴露组PI与暴露时间和血锰的关系采用Pearson相关性分析.8例锰暴露工人1年前后2次MR检查的PI及NAA/Cr比值比较采用t检验.结果 锰暴露组1 8例工人常规头颅MRI中14例表现为双侧对称性分布的T1WI高信号,T2WI信号正常.对照组和锰中毒组受试者常规头颅MRI均未见T1WI高信号.锰暴露组PI值为1.16±0.09,高于中毒组（1.05±0.07）和对照组（1.01±0.05）,差异有统计学意义（F=24.79,P=0.000）.锰暴露组、锰中毒组和对照组血锰浓度分别为（0.051±0.024）、（0.047±0.018）、（0.043±0.020）μg/ml,均未超过正常参考值上限（〈0.10μg/ml）,并且3组间血锰浓度比较差异无统计学意义（F=0.623,P=0.541）.锰暴露组PI与锰暴露时间长短呈正相关（r=0.67,P=0.002）,与血锰无相关（r=0.20,P=0.427）.1H-MRS检查中,锰中毒组NAA/Cr值（1.22±0.07）有一定程度下降,与锰暴露组（1.33±0.13）和对照组（1.31±0.13）间差异有统计学意义（F=4.120,P=0.023）,Cho/Cr、mI/Cr值在各组间差异无统计学意义（P值均〉0.05）.8例锰暴露工人1年后复查PI和NAA/Cr值,与1年前相比差异均无统计学意义.结论 锰暴露工人脑T1WI高信号,PI升高可能是职业性锰暴露致中枢神经系统损伤的生物学指标.

Objective MRI and MR hydrogen proton spectroscopy （1H-MRS） were used to detect the abnormal signal and alteration of metabolites, in order to explore the efficacy of these method in evaluating the damages of central nervous system （CNS） induced by occupational manganese exposure.Methods Eighteen workers exposed to manganese without any manganism symptoms, 12 workers with slightly chronic manganese poisoning, and 19 healthy workers were scanned using routine MRI sequence and 1H-MRS.The blood manganese concentration was also collected for each subject.On cerebral axial T1 WI,the signal intensities of ipsilateral globus pallidus and frontal white matter were measured in the visually brightest area （try to select the signal homogeneous region）, and the globus pallidus index （PI） was then calculated.The 1H-MRS data was calculated to get the values of the peak height of N-acetylaspartate （NAA）, choline （Cho）, inositol （mI） and creatine （Cr） and the ratios of NAA/Cr, Cho/Cr, and mL/Cr were also calculated.One way ANOVA was used to compare the values of PI, NAA/Cr, Cho/Cr, mI/Cr and MnB among the three groups, and the correlations between PI and the time span of manganese exposure or blood manganese concentration were analyzed by Pearson correlation analysis.Eight workers exposed to manganese were followed up one year, and their PI , NAA/Cr before and after follow-up were compared by t test.Results Fourteen of 18 cases exposed to manganese without any manganism symptoms showed symmetrically high intensity signal on T1 WI, while the T2 WI were normal.No high signal intensity was observed on T1WI in any of the healthy workers or manganese poisoning workers.We found that the average PI in manganese exposed group （1.16 ±0.09） was significantly higher （F =24.79 ,P =0.O00）than those of the poisoning （ 1.05 ± 0.07 ） and control groups （ 1.01 ± 0.05 ）.The blood manganese concentration in manganese exposed group, the poisoning group and the control group were （0.051 ±0.024）, （0.047 ±0.018 ）, （ 0.043 ± 0.020 ） μg/ml respectively, which was not significantly different （ F =0.623, P =0.541 ） and did not exceed the upper limit of normal reference value （ 〈 0.10 μg/ml ）.There was a significantly correlation between PI and the time span of manganese exposure （ r = 0.67, P = 0.002 ）,however, there was no correlation between PI and blood manganese concentration （ r = 0.20, P = 0.427 ）.Furthermore, the NAA/Cr ratio decreased variously in the manganese poisoning group （ 1.22 ± 0.07 ） which was significantly lower（ F = 4.120, P = 0.023 ） than those of the poisoning（ 1.33 ± 0.13 ） and control groups （ 1.31 ±0.13）.No statistical significanees were found in the ratios of Cho/Cr and mI/Cr among these three groups（P〉0.05）.No obvious changes of the PI and NAA/Cr were found in the 8 manganese exposed workers after 1 year follow-up.Conclusion Manganese exposure could lead to the high intensity signal on T1 WI, therefore the increased PI may be the biomarkers of central nerve system damages caused by the occupational manganese exposure.