Perl Daniel P, Olanow C Warren
Department of Pathology, Mount Sinai School of Medicine, New York, NY 10029-6574, USA.
J Neuropathol Exp Neurol. 2007 Aug;66(8):675-82. doi: 10.1097/nen.0b013e31812503cf.
Manganese is an essential trace metal that is widely used in industry, particularly in the manufacture of steel. Exposure to high levels of manganese can cause neurotoxicity with the development of a form of parkinsonism known as manganism. It has recently been hypothesized that manganese exposure might also cause or accelerate the development of Parkinson disease (PD). This article is a review of the pathologic studies that have been reported in patients with manganism and in primates experimentally intoxicated with manganese. They demonstrate a consistent pattern characterized by damage to the globus pallidus (particularly the internal segment) with sparing of the substantia nigra pars compacta and the absence of Lewy bodies. This finding contrasts with what is seen in PD, in which there is preferential degeneration of dopamine neurons in the substantia nigra pars compacta coupled with Lewy bodies and preservation of the pallidum. These pathologic findings do not support the notion that manganese causes PD but rather argues that manganese-induced parkinsonism and PD are distinct and separate disease entities.
锰是一种必需的痕量金属，广泛应用于工业，尤其是钢铁制造。接触高浓度的锰会导致神经毒性，并引发一种称为锰中毒的帕金森氏症。最近有假说认为，接触锰也可能导致或加速帕金森病（PD）的发展。本文是对锰中毒患者和实验性锰中毒灵长类动物的病理研究报告的综述。这些研究显示出一种一致的模式，其特征是苍白球（特别是内段）受损，黑质致密部未受影响且无路易小体。这一发现与帕金森病所见情况形成对比，帕金森病中黑质致密部的多巴胺神经元优先退化，伴有路易小体，而苍白球则得以保留。这些病理发现不支持锰导致帕金森病的观点，而是表明锰诱导的帕金森氏症和帕金森病是不同的疾病实体。
