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PET Study of Microglial Activation in Kleine-Levin Syndrome
Lucie Barateau1, Anis Krache1, Alexandre Da Costa1
1From the Sleep-Wake Disorders Unit (L.B., S.C., Y.D.), Department of Neurology, Gui-de-Chauliac Hospital, CHU Montpellier; National Reference Centre for Orphan Diseases, Narcolepsy, Idiopathic Hypersomnia, and Kleine-Levin Syndrome (L.B., Y.D.), Montpellier; Institute of Neurosciences of Montpellier (L.B., S.B., I.J., Y.D.), University of Montpellier, INSERM; ToNIC (A.K., A.D.C., A.-S.S., P.P.), Toulouse NeuroImaging Center, UMR 1214, INSERM, Université Paul-Sabatier; Pediatric Sleep Centre (M.L.), Hospital Robert-Debré; National Reference Centre for Orphan Diseases, Narcolepsy, Idiopathic Hypersomnia, and Kleine-Levin Syndrome (M.L.), Paris; CHRU de Tours - UMR 1253 iBraiN (N.A., P.V.), Université de Tours, Inserm, Inserm CIC 1415; Radiopharmacy Department (M.A., A.-S.S.), CHU Toulouse; Department of Nuclear Medicine (D.M.-G.), CHU Montpellier; PhyMedExp (D.M.-G.), University of Montpellier, INSERM, CNRS; and Nuclear Medicine Department (P.P.), CHU Toulouse, France.
Objectives:
Kleine-Levin syndrome (KLS) is a rare recurrent hypersomnolence disorder associated with cognitive and behavioral disturbances, of unknown origin, but inflammatory mechanisms could be involved. We aimed to explore in vivo microglia activation using [18F]DPA-714 PET imaging in patients with KLS compared with controls, and during symptomatic vs asymptomatic periods.
Methods:
Patients with KLS and controls underwent a standardized clinical evaluation and PET imaging, using a radiolabeled ligand specific to the 18 kDa translocator protein. Images were processed on the PMOD (peripheral module) interface using a standard uptake value (SUV). Five regions of interest (ROIs) were analyzed: hypothalamus, thalamus, frontal area, cerebellum, and whole brain. SUV ratios (SUVr) were calculated by normalizing SUV with cerebellum uptake.
Results:
Images of 17 consecutive patients with KLS (7 during episodes, 10 out of episodes) and 14 controls were analyzed. We found no SUV/SUVr difference between KLS and controls, between patients in and out episodes in all ROIs, and no correlation between SUVr and episode duration at the time of PET scan. No association was found between SUVr and sex, disease duration, or orexin levels.
Discussion:
Our findings do not support the presence of neuroinflammation in KLS. Further research is needed to identify relevant biomarkers in KLS.
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