【作者】 方珊；

【导师】 刘建仁；

【作者基本信息】 浙江大学 ， 脑血管病， 2011， 硕士

【摘要】 研究背景与目的1,2—二氯乙烷是一种在工业上广泛使用的有机溶剂,具有慢性致癌作用,其急性或亚急性吸入可导致中毒性脑病。急性中毒常由事故引起,报道较多。亚急性中毒,由于其潜伏期长,起病隐匿,初期症状常不典型,临床上往往会误诊为神经系统的其它疾病。本文试图通过探讨1,2—二氯乙烷中毒性脑病的临床与影像学特点,提高我们对该病的认识和诊断水平。对象与方法回顾性分析于1998年1月1日至2009年6月30日在浙江大学第二附属医院神经内科住院并确诊为1,2—二氯乙烷中毒性脑病的患者,并对其临床及影像学资料进行分析,总结1,2—二氯乙烷中毒性脑病的临床及影像学特点,为治疗及预后的判断提供一定的依据。结果本组5例患者,均有头痛的临床表现,3例有恶心呕吐,3例有头晕,1例表现为全身肌阵挛,1例表现为全面性强直阵挛性发作,1例有短期记忆缺失,1例有视物模糊。MRI平扫及DWI序列提示弥漫性血管源性水肿中,4例累及双侧苍白球,4例累及皮层下白质,1例累及双侧齿状核,1例为弥漫性细胞源性水肿,主要累及双侧胼胝体。所有患者均经过类固醇和/或甘露醇的治疗后,获得了部分或完全的康复。结论1.1,2二氯乙烷中毒性脑病通常以急性或亚急性起病,其最常见的临床症状为头痛头晕,恶心呕吐,亦可表现为脑局灶性或全面性损害,如肌阵挛、癫痢、意识障碍等。2.脑水肿是1,2二氯乙烷中毒性脑病影像学的重要特征,也是其颅高压的重要病理机制。通过对DWI和ADC的比较分析,可以发现大多数患者为血管源性脑水肿,少数为细胞源性脑水肿或混合性脑水肿。3.对于1,2二氯乙烷中毒性脑病患者,及时给予降颅压,减轻脑水肿的治疗是非常必要的,通常,患者会因此有一个比较好的预后。而作为我们医生,应加强对有关职业病的认识,随时准备好应对随时代发展而来的职业健康危机。更多还原

【Abstract】 Background1,2-Dichloroethane (DCE) is a commonly used industrial solvent. Occupational exposure to DCE may lead to acute DCE toxic encephalopathy.Zhejiang province is one of the fastest developing regions in China with many manufacturing factories such as shoemaking, handicrafts and electronics production in which DCE is commonly used. As a result, there is a high potential for workers to experience occupational exposure to DCE.PurposeTo investigate the clinical and radiological features as well as to improve our knowledge and diagnostic level of toxic encephalopathy caused by occupational exposure to 1,2-Dichloroethane. MethodWe reviewed 5 patients admitted to the department of Neurology in our hospital between January 1st 1998 and June 30th 2009, who were subsequently diagnosed with DCE toxic encephalopathy. The clinical manifestations and imaging features were analyzed.ResultsThe patients’ symptoms included headache (5/5,100%), nausea and vomiting (3/5, 60%), dizziness (3/5,60%), generalized myoclonus (1/5,20%), generalized tonicoclonic seizures (1/5,20%), recent amnesia (1/5,20%), and blurred vision (1/5,20%). The results of cranial MR imaging (MRI) and diffusion weighted MR imaging (DWI) showed extensive cytotoxic edema (1/5,20%), and extensive vasogenic edema in the bilateral globus pallidus (4/5,80%), subcortical white matter (WHM) (4/5,80%), and bilateral nuclei dentatus (1/5,20%), or cytotoxic edema in the corpus callosum (1/5, 20%). All patients were treated with steroids and/or mannitol for 3 to 10 weeks and made either a partial or complete recovery.Conclusions1. It was found that DCE toxic encephalopathy was mostly acute and subacute in onset. The most common clinical features were headache, dizziness, nausea and vomiting. Generalized myoclonus and generalized tonicoclonic seizures are also found in the reports.2. Brain edema was the main neuroimaging feature and the cause of intracranial hypertension in patients with DCE toxic encephalopathy. DWI and ADC mapping showed that most of the patients had vasogenic brain edema, while some had cytotoxic edema or mixed edema. 3. Treatment aimed at reducing ICP and alleviating edema should be given promptly. which can leads to a good outcome.更多还原