• Clin Neurophysiol · Aug 2007

    Cutaneous silent period in patients with restless leg syndrome.

    • Jin-Kyu Han, Kyungmi Oh, Byung-Jo Kim, Seong-Beom Koh, Ju-Yeon Kim, Kun-Woo Park, and Dae-Hie Lee.
    • Department of Neurology, Korea University Medical Center, Korea University College of Medicine, #126-1, Anam-Dong 5Ga, Seongbuk-Gu, Seoul 136-705, Republic of Korea.
    • Clin Neurophysiol. 2007 Aug 1; 118 (8): 1705-10.

    ObjectiveTo investigate the pathophysiological relationship between RLS and small fiber neuropathy using the cutaneous silent period (CSP), which is a spinal reflex mediated by Adelta cutaneous afferents and is useful for the evaluation of small-diameter nerve function.MethodsThe CSP was measured from the extensor digitorum brevis in 157 patients with RLS and 60 healthy controls. The CSP measurement was repeated in the RLS patients after dopamine agonist treatment for one month. The RLS rating scale for clinical severity was used to evaluate each patient before and after treatment. The measured CSP variables were compared between the patient group and the control group. In addition, the possible correlation between the CSP variables and the RLS rating scale score related to treatment was analyzed.ResultsThe mean CSP latencies did not differ between the RLS patients and the healthy controls; however, the mean CSP duration was significantly longer in the RLS patients than in the controls, and this prolonged CSP duration improved to the level of the control subjects after dopamine agonist treatment (p=0.003). The mean RLS rating scale score also significantly decreased after medication (p=0.000). However, the changes in the CSP variables did not correlate with the decrement in the RLS rating scale score.ConclusionsAlthough our results do not support the role of Adelta fiber dysfunction in RLS, the observed change in CSP duration may be useful as a clinical measure of the improvement with dopamine agonist treatment in patients with RLS.SignificanceFurther study is needed to elucidate the exact mechanism involved in the prolonged CSP duration in response to treatment.

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