CHRONIC MANGANESE POISONING - A NEUROPATHOLOGICAL STUDY WITH DETERMINATION OF MANGANESE DISTRIBUTION IN THE BRAIN
CHRONIC MANGANESE POISONING - A NEUROPATHOLOGICAL STUDY WITH DETERMINATION OF MANGANESE DISTRIBUTION IN THE BRAIN
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DOI：
10.1007/bf00686083
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发表时间：
1986-01-01
影响因子：
12.7
通讯作者：
TSUKAGOSHI, H
中科院分区：
文献类型：
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作者：
YAMADA, M;OHNO, S;TSUKAGOSHI, H
据报道，一名 52 岁男性患有慢性锰中毒 (CMP) 的尸检病例，确定了锰在大脑中的分布。该患者自 1965 年以来一直在锰矿石破碎厂工作。1967 年，他开始抱怨行走困难和性欲减退。随后，他出现了各种神经精神症状，包括欣快感、情绪失禁、蒙面、言语单调、“鸡巴走路”、肌张力增高、上下肢无力、眼睑震颤、膝跳跳过度等。主要的神经病理变化是基底神经节的变性，其中苍白球受到严重影响。苍白球显示神经细胞损失和变性，其中内侧节段尤为明显，有髓纤维显着减少，星形胶质细胞中度增殖。黑质完好无损。使用无焰原子吸收光谱法测定了本例 CMP 病例大脑中锰的分布，并与对照病例和帕金森病 (PD) 病例进行了比较。对照组和帕金森病患者的平均锰浓度及其在大脑中的分布没有显着差异。目前的 CMP 病例显示大脑中锰的平均浓度没有升高。但其分布发生了一些变化。因此，CMP 中神经系统疾病的持续存在与大脑中锰浓度本身升高无关。 CMP 在神经病理学和大脑中的锰行为方面似乎与 PD 不同。
An autopsy case of a 52-year-old man suffering from chronic manganese poisoning (CMP) is reported with determination of the manganese distribution in the brain. The patient had been working in a manganese ore crushing plant since 1965. In 1967 he began to complain of difficulties in walking and diminished libido. Later, he developed various neuropsychiatric symptoms including euphora, emotional incontinence, masked face, monotonous speech, "cock-walk", increased muscle tone, weakness of upper and lower extremities, tremor of the eye lids, and exaggeration of knee jerks. The major neuropathological change was degeneration of the basal ganglia, in which the pallidum was severely affected. The pallidum disclosed a loss and degeneration of nerve cells, which was especially marked in the medial segment, a prominent decrease of myelinated fibers, and moderate astrocytic proliferation. The substantia nigra was intact. Distribution of manganese in the brain of the present case of CMP was determined using flameless atomic absorption spectrometry and compared with control cases and also a case of Parkinson''s disease (PD). There was no significant difference between the control cases and the case of PD in average concentration of manganese and its distribution in the brain. The present case of CMP showed no elevation in average concentration of manganese in the brain. However, there were some changes in its distribution. Thus, the continuance of neurological disorders in CMP is not linked to an elevated manganese concentration itself in the brain. CMP appears to be different from PD in neuropathology and manganese behavior in brain.