Katsuragi T, Takahashi T, Shibuya K, Nagatomo H, Iwabuchi K
Department of Neurology and Psychiatry, Kanagawa Rehabilitation Center.
Rinsho Shinkeigaku. 1996 Jun;36(6):780-2.
We report a 55-year-old woman who developed symptoms resembling parkinsonism. Her psychiatric symptoms in the early stage, cervical dystonia and tremor increasing on movement were consistent with manganese poisoning. Manganese levels were elevated to 1.5 micrograms/l in the serum (normal; 0.3-1.1 micrograms/l) and to 1.4 micrograms/l in the urine (normal; less than 1.2 micrograms/l). Intravenous infusion of calcium disodium editate (CaEDTA; chelating agent) was followed by the marked excretion of manganese (27.3 micrograms/l) in the urine. These findings support manganese poisoning. Manganese poisoning is a disease which results from chronic exposure to manganese, but the source of manganese exposure remained obscure in this patient. T1-weighted MRI of the brain showed symmetric high signal intensity in the globus pallidus without any abnormality on T2-weighted images. There is a report that manganese induced brain lesions in Macaca fascicularis as revealed by MRI and the fascicularis developed signs of unsteady gait and hypoactivity. The patient responded to treatment with CaEDTA and the second MRI demonstrated regression of abnormal signal intensity. This may be due to enhanced manganese excretion. To our knowledge, this is the first case of probable manganese-induced human parkinsonism whom changes in MRI were noted after treatment with CaEDTA.
我们报告一名55岁出现类似帕金森症症状的女性。其早期的精神症状、颈部肌张力障碍以及运动时加重的震颤与锰中毒相符。血清锰水平升高至1.5微克/升(正常范围;0.3 - 1.1微克/升),尿锰水平升高至1.4微克/升(正常范围;低于1.2微克/升)。静脉输注依地酸钙钠(CaEDTA;螯合剂)后,尿锰显著排出(27.3微克/升)。这些发现支持锰中毒的诊断。锰中毒是一种因长期接触锰而导致的疾病,但该患者的锰接触源仍不明确。脑部T1加权磁共振成像(MRI)显示苍白球对称高信号强度,T2加权图像未见任何异常。有报告称,MRI显示猕猴因锰导致脑部病变,且猕猴出现步态不稳和活动减少的体征。该患者对CaEDTA治疗有反应,第二次MRI显示异常信号强度消退。这可能是由于锰排泄增加所致。据我们所知,这是首例经CaEDTA治疗后MRI出现变化的可能由锰诱发的人类帕金森症病例。