Hyperdopaminergism in lenticulostriate stroke-related restless legs syndrome: an imaging study

Abstract Objective The pathophysiology of restless legs syndrome(RLS) involves a dopaminergicdysregulation that remains poorly understood, with controversial data from the literature. Stroke-related RLS is a rare condition that involves primarily the basal ganglia, the paramedian pons, and the thalamus. Given these elements, we studied dopaminergicmetabolism in patients with RLS secondary to lenticulostriate infarction using structural and nuclear imaging in the striatumipsilateral to the infarction area, as compared to the contralateral side. We hypothesized that dopaminergicmetabolism would be impaired in the striatumipsilateral to stroke. Methods In this observational case-control study, we aimed to prospectively include patients with RLS secondary to lenticulo-striate infarction, for analyses of dopamine dysfunction ipsilateral to stroke as compared to the contralateral striatumand to a control population. Four patients fulfilled inclusion criteria with either de novo RLS or major exacerbation of RLS existing prior to stroke, and all four patients were included. Structural imaging was performed using brain magnetic resonance imaging, and the stroke-induced metabolic modifications were assessed by 18 F-fluorodeoxyglucose ( 18 F-FDG) positron emission tomography (PET). Dopamine reuptake via DAT was explored using 123 I-FP-CIT SPECT. PET with 18 F-FDOPA was used to evaluate the functional integrity of the presynaptic dopaminergicsynthesis. Results The only structure damaged in all patients was the body of the caudate nucleus, right-sided for three and left-sided for one, as illustrated by magnetic resonance imaging. 18 F-FDG PET showed a hypometabolism in the infarcted area, the ipsilateral thalamus, and the contralateral cerebellum. All patients displayed, in the ipsilateral putamen, increased dopaminergictone. Conclusion The present findings suggest that increased dopaminergictone in the striatummay participate in the pathogenesis of RLS. These observations should encourage further research on RLS symptomatic with well-defined lesions as a promising way to further improve our understanding of its pathophysiology.