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From the Departments of Neuroscience & Anatomy (Drs. Connor and Boyer, and S.L. Menzies) and Pathology (Drs. Connor and Boyer, and S.L. Menzies and B. Dellinger), Penn State University College of Medicine, M.S. Hershey Medical Center, Hershey, PA; Department of Neurology (Drs. Allen and Earley), Johns Hopkins Bayview Medical Center, Baltimore, MD; and Department of Neurology (Dr. Ondo), Baylor College of Medicine, Houston, TX. Dr. Boyer is currently affiliated with Department of Pathology, Division of Neuropathology, University of Texas Southwestern Medical School, Dallas.
Address correspondence and reprint requests to Dr. James R. Connor, Department of Neuroscience & Anatomy (H109), Penn State University College of Medicine, Hershey, PA 17033; e-mail: jrc3{at}psu.edu
Objective: To assess neuropathology in individuals with restless legs syndrome (RLS).
Methods: A standard neuropathologic evaluation was performed on seven brains from individuals who had been diagnosed with RLS. The substantia nigra was examined in greater detail for iron staining and with immunohistochemistry for tyrosine hydroxylase and proteins involved in iron management. Five age-matched individuals with no neurologic history served as controls.
Results: There were no histopathologic abnormalities unique to the RLS brains. Tyrosine hydroxylase staining in the major dopaminergic regions appeared normal in the RLS brains. Iron staining and H-ferritin staining was markedly decreased in the RLS substantia nigra. Although H-ferritin was minimally detected in the RLS brain, L-ferritin staining was strong. However, the cells staining for L-ferritin in RLS brains were morphologically distinct from those in the control brains. Transferrin receptor staining on neuromelanin-containing cells was decreased in the RLS brains compared to normal, whereas transferrin staining in these cells was increased.
Conclusions: RLS may not be rooted in pathologies associated with traditional neurodegenerative processes but may be a functional disorder resulting from impaired iron acquisition by the neuromelanin cells in RLS. The underlying mechanism may be a defect in regulation of the transferrin receptors.
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