机构地区:[1]赣南医学院第一附属医院神经内科,江西赣州341000
出 处:《中国职业医学》2020年第5期567-571,共5页China Occupational Medicine
摘 要:目的探讨职业性急性三甲基氯化锡(TMT)中毒致周围神经损害特点。方法回顾性分析16例职业性急性TMT中毒患者的临床表现和神经电生理、纯音听阈、声导抗测试资料,并于出院6个月后对患者进行随访。结果 16例职业性急性TMT中毒患者中,轻、重度中毒患者各6例,中度中毒患者4例。首发症状中,精神行为异常、记忆力下降者7例次,耳鸣、听力下降和视力下降者各5例次,复视和双眼球痛者各2例次。主要症状中,出现意识障碍8例,定向障碍、攻击性行为6例。纠正低血钾后,仍有四肢肌力减退、肌张力减低、腱反射减弱7例,双下肢腹股沟以下触觉减退9例,行走不稳6例。神经电生理检查主要表现为:有9例(占56.3%)患者表现为异常神经-肌电图;重度中毒患者中有4例异常,表现为运动神经、感觉神经轴索、髓鞘均有损害,近端神经也有部分受损;中度中毒患者中有2例异常,表现为感觉神经轴索、髓鞘损害,仅1根腓总神经脱髓鞘损害;轻度中毒患者3例异常,表现为1根腓总神经轴索受损及1根胫神经近端损害,感觉神经中轴索、髓鞘有损害。轻、中、重度中毒的部分患者有脑干听觉诱发电位的Ⅰ波、视觉诱发电位的P100潜伏期延长,波幅降低。81.3%的患者出现感音神经性耳聋。结论职业性急性TMT中毒可致患者肢体运动神经、感觉神经的轴索及髓鞘损害,远、近端神经均可能累及;亦可损害耳蜗毛细胞和视神经。应重视早期治疗TMT所致的周围神经、耳蜗毛细胞和视神经损害。Objective To explore the characteristics of peripheral nerve injury caused by occupational acute trimethyltin chloride(TMT) poisoning. Methods The clinical manifestations and test data of neurotic electrophysiology, pure tone hearing threshold and acoustic immittance in 16 patients with occupational acute TMT poisoning were retrospectively analyzed. The patients were followed up after 6 months of discharge. Results Among the 16 cases of occupational acute TMT poisoning, 6, 4 and 6 cases were with mild, moderate and severe poisoning, respectively. For the firstly appeared symptoms, 7 cases had abnormal mental behavior and memory loss, 5 cases had tinnitus and hearing loss, 5 cases had decreased visual acuity, 2 cases had diplopia and 2 cases had binocular pain. The main clinical manifestations included 8 cases of disturbance of consciousness, and 6 cases of abnormal orientation and aggressive behavior. After correction of hypokalemia, 7 cases of patients had limb muscle weakness, hypomyotonia and weakened tendinous reflect, 9 cases had decreased tactile sensation below the groin in the lower limbs, and 6 cases had instability of walking. The main manifestations of neuroelectrophysiological detection were: 9 patients(accounting for 56.3%) showed abnormal neuroelectromyography, 4 cases of severe poisoning had damaged motor nerve, sensory nerve axon and myelin sheath, and the proximal nerve was also partially damaged. There were 2 cases of moderate poisoning showing abnormal symptoms, the axon and myelin sheath of sensory nerve were damaged, one common peroneal nerve was demyelinated. Three cases of mild poisoning had one common peroneal nerve axon damaged, one proximal tibial nerve damaged, and the axon and myelin sheath of sensory nerve were damaged. Brainstem auditory evoked potential I wave and visual evoked potential P100 latency prolonged and amplitude decreased in some of the patients with mild, moderate and severe poisoning. The sensorineural hearing loss occurred in 81.3% of patients. Conclusion Occupational
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