Objective: To investigate the change in peripheral nervous conduction velocity in patients with occupational chronic mercury poisoning and related influencing factors. Methods: From February 2011 to December 2014, urinary mercury examination and neural electromyography were performed for 104 patients with occupational chronic mercury poisoning. The data on age, type of work, working years of mercury exposure, and past medical history were collected, and peripheral nervous conduction velocity and its correlation with age, working years of mercury exposure, and urinary mercury concentration were analyzed. Results: All the 104 patients with occupational chronic mercury poisoning had a mean of 45.37±9.82 years, median (P(25), P(75)) working years of 7 (3, 11) , and a median (P(25), P(75)) urinary mercury concentration of 88.50 (56.25, 163.03) μg/g Cr. The major clinical manifestations of peripheral nerve injuries were numbness of extremities (20.2%) , hypopselaphesia/hypalgesia or hyperpselaphesia/hyperalgesia (9.6%) , and bone/muscle pain in the extremities (6.7%) . Neural electromyography showed an increase in denervation potential (fibrillation potential or positive sharp wave) and a detection rate of abnormal peripheral nervous conduction velocity as high as 65.4%. The patients with an older age and more working years had a higher incidence rate of abnormal sensory conduction velocity of the ulnar nerve. There were significant reductions in motor and sensory conduction velocities of the median nerve, motor and sensory conduction velocities of the ulnar nerve, motor conduction velocity of the common peroneal nerve, and the sensory conduction velocity of the superficial peroneal nerve (P<0.05) , with the increase in urinary mercury concentration. Conclusion: Patients with occupational mercury poisoning have a high rate of abnormal neural electromyographic findings, which can be used as an important method for early identification of chronic peripheral nerve injuries induced by mercury poisoning. The degree of peripheral nerve injuries increases with the increasing time of mercury exposure and urinary mercury concentration.
目的： 探讨职业性慢性汞中毒患者周围神经传导速度的变化及影响因素。 方法： 于2011年2月至2014年12月，对104例职业性慢性汞中毒的患者进行尿汞、神经肌电图检查，同时收集其年龄、工种、接汞工龄、既往病史等资料，分析职业性慢性汞中毒患者周围神经传导速度及其与年龄、接汞工龄和尿汞浓度的关系。 结果： 104例职业性慢性汞中毒患者平均年龄为（45.37±9.82）岁，工龄M（P(25)，P(75)）为7（3，11.7）年，尿汞M（P(25)，P(75)）为88.50（56.25，163.03）μg/g Cr。周围神经损害的临床表现主要为四肢麻木（20.2%）、触痛觉减退或过敏（9.6%）及骨或四肢肌肉痛（6.7%）；神经肌电图可见失神经电位（纤颤电位或正锐波）增多，周围神经传导速度异常检出率高达65.4%；年龄较大、工龄较长的患者尺神经感觉传导速度的异常发生率较高；随着尿汞水平的增加，正中神经运动和感觉传导速度、尺神经运动和感觉传导速度、腓总神经运动传导速度和腓浅神经感觉传导速度均下降，差异有统计学意义（P<0.05）。 结论： 职业性汞中毒患者的神经肌电图异常率较高，可作为早期发现慢性汞中毒性周围神经损害的重要手段之一；接汞时间越长、尿汞浓度越高，周围神经损害越严重。.
Keywords: Mercury; Nerve EMG; Peripheral nerves; Poisoning.