From 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.
Neurol Neuroimmunol Neuroinflamm. 2024 Jul;11(4):e200263. doi: 10.1212/NXI.0000000000200263. Epub 2024 Jun 17.
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 [F]DPA-714 PET imaging in patients with KLS compared with controls, and during symptomatic vs asymptomatic periods.
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.
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.
Our findings do not support the presence of neuroinflammation in KLS. Further research is needed to identify relevant biomarkers in KLS.
克莱恩-莱文综合征（KLS）是一种罕见的复发性过度嗜睡障碍，与认知和行为障碍有关，其病因不明，但可能涉及炎症机制。我们旨在通过[F]DPA-714 PET 成像，比较 KLS 患者与对照组、症状期与无症状期患者体内小胶质细胞的激活情况。
KLS 患者和对照组接受了标准化的临床评估和 PET 成像，使用一种针对 18 kDa 转位蛋白的放射性配体。使用 PMOD（外围模块）界面上的标准摄取值（SUV）对图像进行处理。分析了 5 个感兴趣区域（ROI）：下丘脑、丘脑、额叶、小脑和全脑。通过用小脑摄取来标准化 SUV，计算 SUV 比值（SUVr）。
分析了 17 例连续 KLS 患者（7 例发作期，10 例缓解期）和 14 例对照者的图像。我们发现在所有 ROI 中，KLS 患者与对照组之间、发作期与缓解期患者之间，以及 SUVr 与 PET 扫描时的发作持续时间之间均无 SUV/SUVr 差异。SUVr 与性别、疾病持续时间或食欲素水平之间无相关性。
我们的研究结果不支持 KLS 存在神经炎症。需要进一步研究以确定 KLS 中的相关生物标志物。
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