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Ann Clin Neurophysiol > Volume 10(2); 2008 > Article
Ann Clin Neurophysiol. 2008; 10(2): 98-100.
What Is the Origin of Restless Legs Syndrome: Central or Peripheral Nervous system? Clinical, Neuroimaging and Neurophysiologic Evidences of Restless Legs Syndrome as a Disorder of Central Nervous System
Ki-Young Jung
Copyright © 2008 The Korean Society of Clinical Neurophysiology
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Restless legs syndrome (RLS) is a sensorimotor neurological disorder in which the primary symptom is a compellingurge to move the legs, accompanied by unpleasant and disturbing sensations in the legs. Although pathophysiologicmechanism of RLS is still unclear, several evidences suggest that RLS is related to dysfunction in central nervous systeminvolving brain and spinal cord. L-DOPA, as the precursor of dopamine, as well as dopamine agonists, plays an essentialrole in the treatment of RLS leading to the assumption of a key role of dopamine function in the pathophysiology ofRLS. Patients with RLS have lower levels of dopamine in the substantia nigra and respond to iron administration. Iron,as a cofactor in dopamine production, plays a central role in the etiology of RLS. Functional neuroimaging studies usingPET and SPECT support a central striatal D2 receptor abnormality in the pathophysiology of RLS. Functional MRIsuggested a central generator of periodic limb movements during sleep (PLMs) in RLS. However, to date, we have nodirect evidence of pathogenic mechanisms of RLS.
Key words: Restless legs syndrome, dopamine, iron, A11 neuron
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