Hyperdopaminergism in Lenticulostriate Stroke-Induced Restless Legs Syndrome: A Neuro Imaging Study (P7.303)

OBJECTIVE: To explore dopaminergic metabolism in lenticulostriate stroke-related restless legs syndrome (RLS) using MRI and isotopic explorations of both glucose and dopamine. BACKGROUND: The role of dopamine in the pathophysiology of RLS remains poorly understood. Dopaminergic agonists are an efficient treatment of RLS, but they might also cause augmentation syndrome. Further, secondary RLS related to stroke has been previously reported in the case of infarction of basal ganglia and adjacent corona radiate, paramedian pons and thalamus with contiguous internal capsule. We explored the dopaminergic metabolism in patients presenting with lenticulostriate stroke-related RLS. DESIGN/METHODS: All patients referred to our sleep disorder center and presenting with stroke-related RLS following infarction of the basal ganglia were prospectively included over a period of one year. Structural imaging was performed using cerebral MRI, whereas the neural metabolism was analysed using PET with 18 F-FDG and brain dopamine was explored using both PET with 18 F-F-DOPA and SPECT with 123 I-FP-CIT. RESULTS: Four patients were included. For MRI study the body of the caudate nucleus was the only structure that was affected in all patients. Metabolic findings showed in all four patients a hypometabolism in the infarction area, in the ipsilateral thalamus and in the contralateral cerebellum. Three patients displayed decreased dopamine transporter binding in the ipsilateral striatum, whereas higher levels of dopamine precursor were observed in the ipsilateral putamen of all four patients. CONCLUSIONS: A systematic study of small lesions associated with RLS may contribute to understanding the pathophysiological mechanisms underlying this condition. In this regard, the body of the caudate nucleus might be an important structure. The isotopic results reinforce the hypothesis of an increased dopaminergic tone in the striatum as part of RLS pathophysiology. Thus, the efficacy with low doses of dopaminergic agonists in RLS could be explained by stimulation of inhibitory D2-like autoreceptors. Disclosure: Dr. Ruppert has nothing to disclose. Dr. Bataillard has nothing to disclose. Dr. Namer has nothing to disclose. Dr. Tatu has nothing to disclose. Dr. Wolff has nothing to disclose. Dr. Velizarova has nothing to disclose. Dr. Hacquard has nothing to disclose. Dr. Killic-Huck has nothing to disclose. Dr. Bourgin has nothing to disclose.