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From the Department of Neurology (Dr. Olanow) and the Division of Neuropathology (Drs. Good and Perl), Mount Sinai Medical Center, New York, NY; the Neurodegenerative Disorders Center (Drs. Shinotoh, Hewitt, Vingerhoets, Snow, and Calne), Division of Neurology, University of British Columbia, Vancouver, BC, Canada; and the Department of Neurology (Dr. Beal), Massachusetts General Hospital, Boston, MA.
Supported by grants from the National Parkinson's Foundation and the Dystonia Medical Research Foundation.
Received February 7, 1995. Accepted in final form June 28, 1995.
Address correspondence and reprint requests to Dr. C. W. Olanow, Mount Sinai Medical Center, Department of Neurology, One Gustave L. Levy Place, Box 1137, New York, NY 10029.
We gave three adult rhesus monkeys seven IV injections of manganese chloride at approximate 1-week intervals. We evaluated neurologic status by serial clinical examinations and performed a levodopa test if the animal developed features of basal ganglia dysfunction. After the animals were killed, we performed neuropathologic, neurochemical, and laser microprobe mass analysis (LAMMA) studies. Two of three animals developed a parkinsonian syndrome characterized by bradykinesia, rigidity, and facial grimacing suggestive of dystonia but not tremor. Neither animal responded to levodopa. Autopsy demonstrated gliosis primarily confined to the globus pallidus (GP) and the substantia nigra pars reticularis (SNr). We detected focal mineral deposits throughout the GP and SNr, particularly in a perivascular distribution. LAMMA studies noted that mineral deposits were primarily comprised of iron and aluminum. The severity of pathologic change correlated with the degree of clinical dysfunction. These studies demonstrate that, in contrast to Parkinson's disease (PD) and MPTP-induced parkinsonism, manganese primarily damages the GP and SNr and relatively spares the nigrostriatal dopaminergic system. Further, the results suggest that Mn-induced parkinsonism can be differentiated from PD and MPTP-induced parkinsonism by the clinical syndrome and response to levodopa. The accumulation of iron and aluminum suggests that iron/aluminum-induced oxidant stress may contribute to the damage associated with Mn toxicity.
NEUROLOGY 1996,46 492-498
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