Dopamine transporter density is decreased in parkinsonian patients with a history of manganese exposure: What does it mean?

• Published in: Movement disorders 2002-05, Vol.17 (3), p.568-575
• Main Authors: Kim, Y., Kim, J.-M., Kim, J.-W., Yoo, C.-I., Lee, C.R., Lee, J.H., Kim, H.K., Yang, S.O., Chung, H.K., Lee, D.S., Jeon, B.
• Format: Article
• Language: English
• Subjects: Biological and medical sciences; Causality; Chemical and industrial products toxicology. Toxic occupational diseases; Cocaine - analogs & derivatives; Corpus Striatum - metabolism; Corpus Striatum - pathology; Diagnosis, Differential; Dopamine - metabolism; Dopamine Plasma Membrane Transport Proteins; dopamine transporter; Humans; idiopathic Parkinson disease; Iodine Radioisotopes; Male; manganese; Manganese - adverse effects; Manganese - blood; Manganese - urine; Medical sciences; Membrane Glycoproteins; Membrane Transport Proteins - analysis; Middle Aged; Nerve Tissue Proteins; Occupational Exposure - adverse effects; Parkinson Disease - diagnostic imaging; Parkinson Disease - etiology; Parkinson Disease - pathology; Parkinson Disease, Secondary - chemically induced; Parkinson Disease, Secondary - diagnostic imaging; Parkinson Disease, Secondary - pathology; parkinsonism; Tomography, Emission-Computed, Single-Photon; Toxicology; Tropical medicine; Various organic compounds; β-CIT SPECT
• ISSN: 0885-3185; 1531-8257
• DOI: 10.1002/mds.10089

Manganese (Mn) exposure can cause parkinsonism. Pathological changes occur mostly in the pallidum and striatum. Two patients with a long history of occupational Mn exposure presented with Mn‐induced parkinsonism. In one patient, magnetic resonance imaging (MRI) showed findings consistent with Mn exposure, and Mn concentration was increased in the blood and urine. However, this patient's clinical features were typical of idiopathic Parkinson disease (PD). Previous pathological and positron emission tomography studies indicate that striatal dopamine transporter density is normal in Mn‐induced parkinsonism, whereas it is decreased in PD. Therefore, we performed [123I]‐(1r)‐2β‐carboxymethoxy‐3β‐(4‐iodophenyl)tropane ([123I]‐β‐CIT) single‐photon emission computed tomography. Severe reduction of striatal β‐CIT binding was indicated, which is consistent with PD. We propose three interpretations: (1) the patients have PD, and Mn exposure is incidental; (2) Mn induces selective degeneration of presynaptic dopaminergic nerve terminals, thereby causing parkinsonism; or (3) Mn exposure acts as a risk of PD in these patients. Our results and careful review of previous studies indicate that the axiom that Mn causes parkinsonism by pallidal lesion may be over‐simplified; Mn exposure and parkinsonism may be more complex than previously thought. Further studies are required to elucidate the relationship between Mn and various forms of parkinsonism. © 2002 Movement Disorder Society