175名二硫化碳作业工人神经肌电图分析

对１７５名二硫化碳作业工人进行神经系统及神经肌电图检查。结果发现，二硫化碳作业工人的神经肌电图改变符合远端轴索病肌电图的特点，神经肌电图检查对二硫化碳作业工人周围神经损伤有早期诊断价值，而且还表现出二硫化碳暴露对周围神经损伤的剂量—效应关系。     

二硫化碳作业工人的神经肌电图及大脑诱发电位研究

本文对96名二硫化碳作业工人进行了神经肌电图测定,并对其中部分工人作了胫后神经体感诱发电位、视觉诱发电位和脑干听觉诱发电位检查。结果发现,二硫化碳作业工人的神经肌电图改变,符合周围神经远端轴索病之特点。胫后神经体感诱发电位结果显示,脊髓传导时间延长,脊髓传导速度减慢,颈髓以上中枢传导时间与对照组相比,无显著差异。视觉诱发电位和脑干听觉诱发电位无明显改变。     

慢性二硫化碳中毒的临床神经电生理研究进展

国内外研究表明神经肌电图能客观和敏感地检测二硫化碳引起的周围神经损伤，大脑诱发电位能检测二硫化碳对感觉传导通路的影响，脑电图可在一定程度上反映二硫化碳所致的中枢神经系统机能紊乱。临床神经电生理技术是诊断慢性二硫化碳中毒的客观和敏感的指标。     

二硫化碳作业工人临床神经电生理研究

目的探讨慢性二硫化碳中毒的早期诊断方法。方法对二硫化碳作业工人进行神经传导速度和脑干听觉诱发电位检测,运用方差分析方法分析检测结果。结果１７５名二硫化碳作业工人与８０例正常人比较,神经传导速度测定１５个参数中的１３个参数差异有显著意义。对５２名二硫化碳作业工人和２６名正常人的脑干听觉诱发电位的分析表明,接触组和对照组、不同工龄组别与对照组间脑干听觉诱发电位Ⅰ、Ⅲ、Ⅴ各主波潜伏时和峰间潜伏时未见差异。结论低水平二硫化碳长期接触对听觉神经传导通路影响不大,二硫化碳作用主要靶部位是周围神经。     

188名二硫化碳作业工人临床与神经电生理分析

对188名二硫化碳作业工人的临床特征及电生理变化进行分析,发现二硫化碳中毒临床表现以头痛、头晕、记忆力减退等中枢神经损害为主,其次为对称性感觉运动型周围神经病,且以上肢运动神经损害明显,脱髓鞘和远端轴索损伤合并存在。 更多还原     

二硫化碳对实验大鼠神经系统神经营养因子的影响

目的探讨二硫化碳染毒对大鼠神经生长因子(NGF)和脑源性神经营养因子(BDNF)蛋白表达的影响。方法健康雄性Wistar大鼠20只随机分成对照组和二硫化碳组,每组10只。二硫化碳组大鼠腹腔注射二硫化碳玉米油溶液,开始4周染毒剂量为150mg/kg,1次/d,6次/周,后4周染毒剂量为300mg/kg,1次/d,6次/周。对照组腹腔注射等剂量的玉米油溶液。染毒结束后对周围神经损伤体征进行评分,同时检测胫神经运动神经传导速度和腓肠神经感觉神经传导速度;并应用免疫组化方法检测NGF、BDNF在海马及坐骨神经中的蛋白表达情况。结果二硫化碳染毒8周后染毒组大鼠周围神经体征评分明显升高;与对照组比较,神经电生理测定结果显示二硫化碳染毒组胫神经运动神经和腓肠神经感觉神经传导速度明显减慢,潜伏期延长,波幅减低。染毒组大鼠海马及坐骨神经中NGF和BDNF表达较对照组显著降低。结论二硫化碳染毒导致的神经组织NGF、BDNF蛋白表达下降可能参与了其神经毒作用。     

二硫化碳接触水平与神经行为功能的剂量效应分析

目的运用多媒体神经行为测试评价系统中文版第三版(NES-C3),探讨二硫化碳(CS2)作业工人神经行为功能与CS2接触水平之间的关系。方法使用NES-C3对81名接触CS2工人的神经行为功能进行测试,并与其接触水平进行相关分析。结果接触二硫化碳水平与负性情绪(困惑—迷惘)呈正相关;与“瞬时记忆能力(记忆扫描准确数)”、“感知—注意力调转”能力等判断能力呈负相关。结论表明接触二硫化碳浓度越高,相应神经行为功能的影响越严重。     

57例二硫化碳作业工人神经肌电图随访研究

目的：探讨二硫化碳对周围神经损伤的发展规律。方法：对长期接触二硫化碳浓度高于国家最高容许浓度１０ｍｇ／ｍ３数倍的５７例工人，１９８９、１９９５年进行临床和神经肌电图检查。结果：６年后，在５７例工人中１８例肯定周围神经病转为可疑或恢复正常。在１２例已脱离接触二硫化碳半年至１７年的工人中，８例仍为肯定周围神经病，２例转为可疑，１例恢复正常。结论：二硫化碳慢性中毒性周围神经病恢复是缓慢的，反映了二硫化碳所致的轴索损伤修复慢的特征。我们主张神经肌电图检查一旦发现周围神经病，应及时脱离以利于神经损伤的恢复     

计算机化神经行为评价系统的研究与进展

神经行为测试具有简便、无创伤、易被接受和比较敏感等优点,在许多领域中应用广泛。继芬兰心理学家Hanninen在60年代初首次采用成套的心理行为方法,对铅、苯、汽油及二硫化碳等作业工人进行接触化学物质与行为功能改变的流行病学观察后,目前,已有许多神经行为测试组合,用于评价职业人     

甲苯的神经毒性

本文从神经行为、神经电生理以及神经生化等方面详细综述了甲苯对人和动物的神经毒性。甲苯可影响脑单胺类神经递质代谢及多种脑酶活性,并能使动物的操作行为和电生理发生改变。工人长期职业接触低浓度的甲苯即有可能出现神经行为功能改变。     

粘胶工人尿2-硫代噻唑烷-4-羧酸浓度与神经传导速度的相关性研究

目的 探讨尿中－2硫代噻唑烷－4－羟酸（TTCA）含量作为内暴露指标在我国二硫化碳（CS2）接触工人神经系统功能职业健康监护方面的实际应用价值。方法 应用高效液相色谱法测定工人8h班末尿TTCA含量,选取尿中TTCA＜5mg/gCr者作为研究对象;应用常规方法测定工人腓总神经和腓肠神经传导速度及腓总神经F波最短潜伏期;用SAS软件包进行多元回归统计分析。结果 暴露组与对照组比较,工人神经传导速度的相关指标存在组间差异：暴露组运动神经元端及近端动作电位波幅降低（偏回归系数分别为－1．0985、－0．9557）,F波最短潜伏期延长（偏回归系数为1．6830）。结论 就周围神经系统功能而言,尿TTCA含量作为我国CS2接触工人的一项敏感的内暴露指标。     

职业性急性二硫化碳中毒病例特点总结

  目的  了解职业性急性二硫化碳中毒病例特点。
  方法  基于CNKI中国学术期刊网络出版总库、万方数字化期刊数据库、Pubmed、Sciencedirect等数据库,收集、筛选国内外职业性急性二硫化碳中毒病例,并将其分为二硫化碳中毒组与二硫化碳、硫化氢混合中毒组,对其临床特征进行总结、分析。
  结果  172例职业性急性二硫化碳中毒患者主要表现为头晕、头痛,恶心、呕吐,乏力,步态蹒跚等症状,检出率分别为94.8%、79.7%、69.8%、41.3%。三颤试验、共济失调阳性率较高,其检出率分别为29.1%、27.9%。辅助检查主要为脑电图异常、心电图异常（心肌缺血）,其检出率分别为9.9%,9.3%。二硫化碳中毒组与混合中毒组三颤试验、脑电图检查阳性率差异有统计学意义（P < 0.05）,其他指标差异无统计学意义（P > 0.05）。
  结论  二硫化碳急性中毒可导致中枢神经、心血管系统及周围神经损害,职业性二硫化碳中毒诊断标准有待进一步完善。
     

Studies on chronic carbon disulfide poisoning

Summary In our previous paper (1967) it was asserted that the pathological and clinical features of chronic carbon disulfide poisoning are microangiopathy (microangiopathia sulfocarbonica) characterized by retinal microaneurysm or nephropathy, which may develop into glomerulosclerosis. This postulation first poses a question, whether or not pathogenesis of the microangiopathy has a similar history to that seen in diabetes mellitus.To elucidate the pathogenesis of microangiopathy due to carbon disulfide, prednisolone augmented glucose tolerance test and fluorescein angiography were carried out in 214 carbon disulfide workers and 45 control workers.Both the one- and two-hour postglucose blood sugar levels during prednisolone GTT were higher in carbon disulfide workers than in controls, and it was certified that these blood sugar levels increased with lengthening of duration of exposure to carbon disulfide. Abnormal prednisolone GTT was found in 21 % of the carbon disulfide workers and in 4.4 % of the controls. Retinal microaneurysm was found in 55.9 % of the former and in 15.4 % of the latter. There was a clear trend toward higher incidence of microaneurysm with increasing duration of exposure to carbon disulfide. In 26 cases out of 109 carbon disulfide workers with retinal microaneurysm, abnormal prednisolone GTT was found (23.9 %). On the other hand, in the controls with microaneurysm, there were no cases with abnormal prednisolone GTT.The results permit the statement that carbon disulfide has a mild diabetogenic action and pathogenesis of retinal microaneurysm due to carbon disulfide is closely related to that seen in diabetes mellitus.     

Carbon disulfide-induced neuropsychiatric changes in grain storage workers

The clinical and neuropsychiatric features of seven workers from the grain storage industry are described. All were exposed to fumigants, especially carbon disulfide and malathion. Clinical manifestations included cogwheel rigidity, resting and action tremor, peripheral neuropathy, pyramidal tract signs, an EEG pattern of sleep apnea, and characteristic measurable neurobehavioral dysfunction. Similar signs and symptoms due to carbon disulfide exposure in the viscose rayon industry strongly supported the conclusion that these grain storage workers were suffering from carbon disulfide poisoning. Malathion exposure probably had a contributing role. We conclude that exposure to these fumigants poses a serious occupational risk to the nervous system.     

长期接触低浓度二硫化碳对暴露人群DNA损伤的影响

目的 应用彗星试验方法检测长期接触低浓度二硫化碳(CS2)职业人群的口腔黏膜细胞DNA损伤以及损伤程度。方法 在湖北省某大型化纤厂随机抽取90例CS2接触工人作为暴露组,同时选择81例非接触工人作为对照组,进行彗星试验。结果 暴露组和对照组的彗星细胞拖尾率分别为0．51％和0．23％,经X^2检验,差异有非常显著性。另外,低作业年限暴露组(0．50％)和男性暴露组(0．56％)的彗星细胞拖尾率均非常显著高于对照组,分别为0．08％和0．25％。多因素非条件logistic回归分析结果表明,CS2暴露组DNA损伤的可能性明显高于对照组。结论 长期接触低浓度CS2,对工人口腔黏膜细胞的DNA有一定损伤。     

二硫化碳对大鼠周围神经轴浆运输和能量代谢的毒作用效应

为研究二硫化碳（ＣＳ２）对周围神经系统的毒作用效应，用亚慢性染毒方式建立ＣＳ２所致周围神经病的大鼠模型后，采用同位素示踪技术和反向高效液相色谱法（ＲＰ－ＨＰＬＣ），分别测定了染毒组和对照组大鼠的坐骨神经中轴浆运输和能量代谢的变化。结果显示，同位素标记物３Ｈ－亮氨酸在亚慢性ＣＳ２中毒大鼠坐骨神经的运动和感觉神经中的运行距离均比对照组短；坐骨神经中ＡＴＰ、ＡＤＰ和ＡＭＰ的含量也均低于对照组。本研究表明ＣＳ２引起大鼠的周围神经损伤出现轴浆运输和能量代谢功能障碍。这些改变与ＣＳ２中毒性周围神经病在时间－剂量－反应上的关系尚待深入研究。     

An epidemiological study on retinopathy due to carbon disulfide

Summary In order to clarify the influence of carbon disulfide exposure level on the progress of retinopathy, direct ophthalmoscopy and color fundus photography were performed on 338 randomly-selected workers of a viscose rayon staple plant.Retinal abnormalities characterized by microaneurysms were found in 89 of 289 workers exposed to carbon disulfide (30.8%) and in 2 of 49 control workers not exposed to carbon disulfide (4.1%). The prevalence of retinopathy among 124 high exposure group members was significantly higher than that among 127 low exposure group members. Results clearly showed that the prevalence of retinopathy increased with both increasing carbon disulfide exposure duration and increasing concentration.Finally, the onset and progress of retinal changes due to carbon disulfide are compared to those occuring with diabetes mellitus.     

Electrophysiological studies on rabbits in long-term exposure to carbon disulfide.

Electroneuromyography was performed as part of a multidemensional study of experimental carbon disulfide poisoning of rabbits. Ten rabbits were exposed by inhalation of 750 ppm of carbon disulfide for 6 hours a day, 5 days a week for 10 weeks. A slowing of the motor conduction velocity of the sciatic nerve was clearly observable during the course of exposure. This slowing preceded clinical paralysis, which became severe in the hind limbs within 9 weeks. Although the amplitude of the motor response to stimulation diminished markedly towards the end of the exposure period, a response of about 2 mV was always elicitable. Definite fibrillations could be noted in the gastrocnemius muscle of the rabbits after exposure for 9 weeks. In the two rabbits allowed to recover, the fibrillations continued for up to 2 months after the cessation of the carbon disulfide exposure. As the paralysis was very severe, even though the nervous conductivity was rather well preserved, it was assumed that a lesion at the spinal cord level was combined with neuropathy. These experimental findings from rabbits agreed well with results from clinical studies of workers occupationally exposed to carbon disulfide. Some similarities, but also differences, were observable between neurophysiological findings in carbon disulfide and other forms of experimental toxic neuropathy.