Striatal mechanism of the restless legs syndrome.

Striatal mechanism of the restless legs syndrome.
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不宁腿综合征的纹状体机制。

DOI:
10.1093/sleep/zsac110
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发表时间:
2022
期刊:
影响因子:
5.6
通讯作者:
Siegel,JeromeM
Siegel,JeromeM
中科院分区:
医学2区
文献类型:
--
作者:
Lai,Yuan-Yang;Hsieh,Kung-Chiao;Chew,Keng-Tee;Nguyen,Darian;Siegel,JeromeM

文献摘要

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研究目的据报道,脑铁缺乏与不宁腿综合征(RLS)有关。然而,30%-50%的RLS患者对铁治疗没有反应,这表明除了脑铁缺乏之外的机制也可能参与该疾病。纹状体参与了运动活动的调节。我们推测纹状体功能障碍可能会诱发RLS。方法采用野生型(WT)大鼠和缺铁(ID)大鼠两组。各组分为对照组和n -甲基-d-天冬氨酸纹状损伤组。基线记录后,给纹状损伤野生型(WT-STL)和纹状损伤缺铁型(ID-STL)大鼠注射普拉克索和硫哌丁胺。然后给缺铁和ID-STL大鼠标准啮齿动物饮食4周,记录它们的睡眠和运动活动。结果swt - stl大鼠醒时周期性腿动(PLM)增加,慢波睡眠时周期性腿动(PLM)增加,慢波睡眠时快速眼动睡眠减少,慢波睡眠时平均发作时间缩短。睡眠-觉醒模式和运动活动在ID和ID- stl大鼠之间没有差异。硫哌丁胺或普拉克索注射液降低WT-STL大鼠和ID-STL大鼠睡眠和清醒时PLM。与ID大鼠的运动多动可以通过补铁得到逆转不同,ID- stl大鼠的醒时和睡眠时PLM并没有通过补铁得到完全纠正。结论大鼠纹状体损伤可产生类似rls的活动。纹状体功能障碍可能是导致一些人类RLS患者对铁治疗无效的原因。
Study ObjectivesBrain iron deficiency has been reported to be associated with the restless legs syndrome (RLS). However, 30%–50% of RLS patients do not respond to iron therapy, indicating that mechanisms other than brain iron deficiency may also participate in this disease. The striatum is known to be involved in the modulation of motor activity. We speculated that dysfunction of the striatum may induce RLS.MethodsTwo groups, wild-type (WT) and iron-deficient (ID) rats were used. Each group was divided into two subgroups, control andN-methyl-d-aspartate striatal-lesioned. After baseline recording, striatal-lesioned wild-type (WT-STL) and striatal-lesioned iron-deficient (ID-STL) rats were given pramipexole and thioperamide injections. Iron-deficient and ID-STL rats were then given a standard rodent diet for 4 weeks, and their sleep and motor activity were recorded.ResultsWT-STL rats showed periodic leg movements (PLM) in wake, an increase in PLM in slow wave sleep (SWS), a decrease in rapid-eye-movement sleep, and a decrease in the daily average duration of episodes in SWS. The sleep–wake pattern and motor activity did not differ between ID and ID-STL rats. Thioperamide or pramipexole injection decreased PLM in sleep and in wake in WT-STL rats and ID-STL rats. Unlike ID rats, whose motor hyperactivity can be reversed by iron replacement, PLM in wake and in sleep in ID-STL rats were not fully corrected by iron treatment.ConclusionsLesions of the striatum generate RLS-like activity in rats. Dysfunction of the striatum may be responsible for failure to respond to iron treatment in some human RLS patients.