ArticleSleep2022
Striatal mechanism of the restless legs syndrome.
Article in Sleep, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it, 5 citations in OpenAlex.
- Putative Animal Models of Restless Legs Syndrome: A Systematic Review and Evaluation of Their Face and Construct Validity.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Pooled it
- Multidimensional iron dysmetabolism and gut-brain axis interactions in restless legs syndrome: from peripheral deficiency to central dysregulation.Frontiers in aging neuroscience · 2026Review
- The correlation between RLS and motor or other non-motor symptoms of PD patients: an observational study.BMC neurology · 2025Observational
- Effects of iron-deficient diet on sleep onset and spinal reflexes in a rodent model of Restless Legs Syndrome.Frontiers in neurology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
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 and N-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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.