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Sleep–Wake Disorders
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Margaret Kay-Stacey, Eunice Torres-Rivera, Phyllis C. Zee
Symptoms in idiopathic hypersomnia (IH) include the following:43EDS.Significant sleep inertia or ‘sleep drunkenness' in the morning, making it very difficult to wake up.Naps may be short and restorative or long and unrefreshing. Majority of IH patients report the latter (87% report long naps > 60 minutes; 52–78% consider their naps unrefreshing; may have associated postnap sleep inertia).Nighttime sleep is normal or long (> 10 hours).May have associated symptoms such as trouble focusing, headaches, orthostatic hypotension, etc.
Update on treatment for idiopathic hypersomnia
Published in Expert Opinion on Investigational Drugs, 2018
Elisa Evangelista, Régis Lopez, Yves Dauvilliers
Idiopathic hypersomnia (IH) is an orphan disease responsible for severe excessive daytime sleepiness (EDS), prolonged nighttime sleep, and sleep inertia [1,2]. The lack of specific biomarkers together with the absence of well-designed controlled studies with homogeneous inclusion criteria contribute to weak epidemiological, clinical, and pathophysiological characterizations of IH. IH is often associated with major functional impairments in various domains and impaired quality of life, similar to that of narcoleptic patients [3–5]. Symptoms of IH may be severe and long lasting, but spontaneous improvement and remission have been reported in up to 33% of patients [6–8]. No cure exists for IH, and most patients require long-term symptomatic treatment. To date, only three recent randomized, double-blind, placebo-controlled trials have been conducted in IH, two for modafinil and one for clarithromycin. For the other pharmacological treatments, the majority of available data are provided by observational studies and case series. Recently, the French Sleep Medicine and Research Society established the first guidelines for the assessment and treatment of IH, with only grade B and C recommendations due to insufficient levels of evidence [9]. Pharmacological treatments commonly prescribed for IH are stimulant drugs being approved for narcolepsy by the European Medicine Agency (EMA) or the US Food and Drug Administration (FDA). However, all these medications are used off-label for the management of EDS in IH.
Development of a lower-sodium oxybate formulation for the treatment of patients with narcolepsy and idiopathic hypersomnia
Published in Expert Opinion on Drug Discovery, 2022
Gunjan Junnarkar, Clark Allphin, Judi Profant, Teresa L. Steininger, Cuiping Chen, Katie Zomorodi, Roman Skowronski, Jed Black
Idiopathic hypersomnia is another serious sleep disorder characterized by EDS in all patients, as well as sleep inertia (defined as prolonged difficulty waking with frequent reentries into sleep, confusion, and irritability), prolonged nighttime sleep, cognitive impairment, and long, unrefreshing naps in many patients [10–12]. Like narcolepsy, idiopathic hypersomnia is a chronic, debilitating disease with no cure (although the severity may vary over time, and spontaneous remissions can occur). Pharmacotherapy for idiopathic hypersomnia has typically involved the same treatments that are used for narcolepsy [11].
Pharmacotherapy of residual excessive sleepiness among continuous positive airway pressure (CPAP) treated patients with sleep apnea
Published in Expert Opinion on Pharmacotherapy, 2022
Ali A. El-Solh, Avantika Rudraraju, Divij Pasrija, Hoang Bui
Depression is highly comorbid with EDS and has a bidirectional relationship with OSA [32,33]. The coexistence of depression can be easily probed with a brief depression inventory. In one study comprising all referrals for OSA evaluation, 41% of patients exhibited mild symptoms of depression and 12% had moderate-to-severe symptoms [34]. More importantly, 38.8% of CPAP non-adherent patients had a history of depression [15]. Narcolepsy is a chronic debilitating disorder associated with loss or dysfunction of the wake-promoting hypothalamic hypocretin system likely as a result of an auto-immune response [35]. The condition may present with or without cataplexy. Evaluation for narcolepsy is entertained in the context of persistent sleepiness despite CPAP adherence considering that the prevalence of OSA in narcoleptics ranges from 24% to 68% [36,37]. In some instances, the diagnosis of narcolepsy is uncovered only after reevaluation for residual EDS [38]. Similarly, idiopathic hypersomnia may only be revealed after patients continue to complain of residual sleepiness despite adequately treated OSA. However, unlike narcolepsy, patients with idiopathic hypersomnia report reduced alertness, prolonged nocturnal sleep time, and unrefreshing daytime naps. The diagnosis is established by excluding all other disorders associated with EDS and documenting a mean sleep latency of less than or equal to 8 min with less than two sleep-onset rapid eye movement (SOREM) episodes on the Mean Sleep Latency Test (MSLT) or a total 24-hour sleep time ≥660 minutes on 24-hour polysomnography or by wrist actigraphy. Last but not least, shift work sleep syndrome is a well-recognized cause of EDS estimated to affect about 10% of those who work irregular hours [39]. Working beyond the normal daylight shift disrupts the circadian sleep-wake cycle and decreases both the quality and efficiency of sleep. On the other hand, recurrence of EDS following successful treatment usually indicates worsening of underlying OSA due to weight gain or emergence of a new or previously undiagnosed condition. In both instances of residual EDS, whether it is unremitting or arising do novo, the approach to diagnostic testing is predicated on both disease manifestation and temporal evolution of symptoms.