Absence of pontine lesions in narcolepsy. Pontine lesions in idiopathic narcolepsy. Plazzi G, Montagna P, Provini F, Bizzi A, Cohen M, Lugaresi E. Circuit mechanisms of sleepiness and cataplexy in narcolepsy. Increased GABAergic efficacy of central amygdala projections to neuropeptide S neurons in the brainstem during fear memory retrieval. Jungling K, Lange MD, Szkudlarek HJ, Lesting J, Erdmann FS, Doengi M, et al. Sleep disorders, obesity, and aging: the role of orexin. Nixon JP, Mavanji V, Butterick TA, Billington CJ, Kotz CM, Teske JA. Hypothalamic hypocretin (orexin): robust innervation of the spinal cord. Reduced number of hypocretin neurons in human narcolepsy. Thannickal TC, Moore RY, Nienhuis R, Ramanathan L, Gulyani S, Aldrich M, et al. A mutation in a case of early onset narcolepsy and a generalized absence of hypocretin peptides in human narcoleptic brains. Peyron C, Faraco J, Rogers W, Ripley B, Overeem S, Charnay Y, et al. Saper CB, Fuller PM, Pedersen NP, Lu J, Scammell TE. The sleep switch: hypothalamic control of sleep and wakefulness. Neurons containing hypocretin (orexin) project to multiple neuronal systems. Peyron C, Tighe DK, van den Pol AN, de Lecea L, Heller HC, Sutcliffe JG, et al. Hypothalamic regulation of sleep and circadian rhythms. Evidence of a perceptual-encoding deficit in narcolepsy? Sleep. Sustained attention to response task (SART) shows impaired vigilance in a spectrum of disorders of excessive daytime sleepiness. Van Schie MK, Thijs RD, Fronczek R, Middelkoop HA, Lammers GJ, Van Dijk JG. Attention deficits in patients with narcolepsy. Executive attention and working memory in narcoleptic outpatients. Neuroimaging correlates of narcolepsy with cataplexy: a systematic review. Wada M, Mimura M, Noda Y, Takasu S, Plitman E, Honda M, et al. Cambridge: Cambridge University Press 2013. Neuroimaging of sleep and sleep disorders. In: Nofzinger E, Maquet P, Thorpy M, editors. Narcolepsy, 2nd edition: a clinical guide. Neuroimaging of narcolepsy and primary hypersomnias. Central disorders of hypersomnolence: focus on the narcolepsies and idiopathic hypersomnia. Diagnosis of central disorders of hypersomnolence: a reappraisal by European experts. Lammers GJ, Bassetti CLA, Dolenc-Groselj L, Jennum PJ, Kallweit U, Khatami R, et al. To split or to lump? Classifying the central disorders of hypersomnolence. 2009 32(6):753–9.įronczek R, Arnulf I, Baumann CR, Maski K, Pizza F, Trotti LM. Idiopathic hypersomnia with and without long sleep time: a controlled series of 75 patients. Longstreth WT Jr, Koepsell TD, Ton TG, Hendrickson AF, van Belle G. Mahlios J, De la Herran-Arita AK, Mignot E. International classification of sleep disorders-third edition: highlights and modifications. Papers of particular interest, published recently, have been highlighted as: In addition, multi-modal imaging methods will be crucial to resolve previous inconsistencies and identify reliable objective biomarkers that could aid in understanding the pathophysiology and potentially support the diagnostic process. Larger studies with consistent clinical phenotyping should be the focus of future investigations. Most neuroimaging studies to date have been conducted in small samples, while narcolepsy type 2 (or narcolepsy without cataplexy) and idiopathic hypersomnia remain relatively understudied. Finally, recent studies suggest a disruption of the default-mode network in patients with idiopathic hypersomnia. Functional studies have mainly focused on resting-state or emotion regulation in narcolepsy type 1 and have revealed disturbed activity in limbic and mesolimbic structures in relation to cataplexy. Most studies have focused on narcolepsy type 1 (or narcolepsy with cataplexy), showing inconsistent but extensive structural differences in the hypothalamus and its normally widespread projections. Here, we review current structural and functional brain imaging findings in central hypersomnolence disorders and discuss the future perspectives of neuroimaging in these sleep disorders. Neuroimaging techniques have provided valuable insights into the pathophysiology of narcolepsy and idiopathic hypersomnia. Clinical presentation of central hypersomnolence disorders, including narcolepsy type 1 and 2 and idiopathic hypersomnia, is often similar, and determining the correct diagnosis remains challenging.
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