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 Welcome. Thank you for joining us. I’m Dr Debra Stultz. I’m a sleep doctor and psychiatrist in Barboursville, West Virginia, at Stultz Sleep & Behavioral Medicine. I’m honored to have Dr Stephen Stahl with us. He is the chairman of the Neuroscience Education Institute and an adjunct professor with the University of California, San Diego [School of Medicine]. He needs no introduction because anybody exposed to this program has grown up in psychiatry, and sleep, and medicine on his books about neurotransmitters and diagrams. You’ve done so much to advance our field. It’s my honor to be here with you, so thank you for joining us.

 Thank you for the kind introduction. I’m glad to be here.

 We’re going to be talking about narcolepsy treatment. Narcolepsy can be a complicated illness, and there are many causes of narcolepsy. Give me your idea about what’s involved in the disorder of narcolepsy from your standpoint?

 A lot of people have traditionally thought about narcolepsy as falling asleep and sleep attacks, and certainly it is that. But why? Why would you fall asleep suddenly? What we’ve learned is the story of this new neurotransmitter that maybe the listeners haven’t heard about in their training or medical school. It’s called orexin. Some people call it hypocretin. It’s interesting, neurologists and psychiatrists call the same thing different terms. But that little sucker lives in the small part of the lateral hypothalamus, and if you have disruption of that part of the brain, it stops making orexin. Why do you care? Because orexin doesn’t make you awake, but it stabilizes wakefulness. Narcolepsy is the destabilization of wakefulness. What ends up happening is you’re not awake; you’re asleep.

You may not know this, but I may have fallen asleep for a microsleep episode ever since I even started this talk. Because if you actually do EEGs [electroencephalograms] on all of us—I’ve seen the EEGs from pilots going in an airplane across the Atlantic. They have microsleep episodes that are fast, and they wake up again because they have good orexin controls. What happens if you lose your orexins? When that little impulse comes to fall asleep, you do. We lose orexins for a number of reasons. I mean, nobody really knows why, but there seems to be a cause of narcolepsy where your immune system goes wild and eats your lateral hypothalamus. You lose your orexins, and then you don’t stabilize wakefulness anymore. It’s a very fascinating illness. You have arousal neurotransmitters and sleep neurotransmitters, but you also have stabilization of arousal neurotransmitters.

 Right. I often describe it to my patients as like a light that flickers on and off. Sometimes it’s on, sometimes it’s off, sometimes it’s just flickering. You have a flickering of sleep into wake during the day, and you have a flickering of wake into sleep at night. It’s an unsteady situation.

Dr Stephen Stahl is clinical professor of psychiatry and neuroscience at the University of California Riverside, adjunct professor of psychiatry at the University of California San Diego, and honorary fellow in psychiatry at the University of Cambridge. Over the past 12 months (January 2020 - December 2020), Dr Stahl has served as a consultant to Acadia, Alkermes, Allergan, AbbVie, Arbor Pharmaceuticals, Axovant, Axsome, Celgene, Concert, Clearview, EMD Serono, Eisai Pharmaceuticals, Ferring , Impel NeuroPharma, Intra-Cellular Therapies, Ironshore Pharmaceuticals, Janssen, Karuna, Lilly, Lundbeck, Merck, Otsuka, Pfizer, Relmada, Sage Therapeutics, Servier, Shire, Sunovion, Takeda, Taliaz, Teva, Tonix, Tris Pharma, and Viforpharma; he is a board member of Genomind; he has served on speakers bureaus for Acadia, Lundbeck, Otsuka, Perrigo, Servier, Sunovion, Takeda, Teva, and Vertex; and he has received research and/or grant support from Acadia, Avanir, Braeburn Pharmaceuticals, Eli Lilly, Intra-Cellular Therapies, Ironshore, ISSWSH, Neurocrine, Otsuka, Shire, Sunovion, and TMS NeuroHealth Centers.

Dr Debra Stultz is the Director and Owner of Stultz Sleep and Behavioral Health in Barboursville, West Virginia. Dr Stultz earned her medical degree from Marshall University School of Medicine in Huntington, West Virginia. She completed a residency in psychiatry and a fellowship in child and adolescent psychiatry through West Virginia University at their Charleston Division through Charleston Area Medical Center in Charleston, West Virginia. She is board certified in psychiatry, sleep medicine, and behavioral sleep medicine. With a special interest in Narcolepsy, she treats a variety of sleep disorders and psychiatric issues. She is also the editor for the Clinical TMS Society newsletter, on their Board of Directors, and the chairman of the TMS and Sleep Disorders Affinity Group. Dr Stultz is on the advisory committee for Harmony Biosciences and is a speaker for Harmony Biosciences and Jazz Pharmaceuticals.

In this custom video series, Stephen Stahl, MD, PhD, discusses the underlining cause of narcolepsy and the role of the neurotransmitter orexin (hypocretin) in the stabilization of wakefulness.

Orexin and the Destabilization of Wakefulness in Narcolepsy

Not long ago, tranquilization was an important goal of psychopharmacology, and sedation was integral to this therapeutic effect. Major tranquilizers (ie, antipsychotics) sedated psychosis and mania, while minor ones (ie, benzodiazepines) calmed the anxious mind. Even antidepressants were thought to 

, in part because insomnia is a symptom of depression, but also because of concerns that patients might act on suicidal impulses if their energy improved before their depression did.

Those ideas were put to rest in the 1990s, as nonsedating medications proved just as effective as their sedating predecessors. Rather than forewarning suicide, early increases in energy and physical activity are actually a 

 Improved functioning is the goal in psychopharmacology, and sedation usually does not contribute to that goal.

Sedation is sometimes desirable and sometimes not. It is desirable when treating 

, as long as the sedative effects do not linger into the morning. It can also be life-saving when treating acute agitation in emergency situations. Increased activity does not foretell a positive outcome, and may even be a risk factor for suicide, when it is due to adverse effects like 

The simplest way to manage unwanted sedation is to choose medications that are less likely to cause it. 

 ranks psychiatric medications by their sedation risk, based on meta-analyses of clinical trials and data from the US Food and Drug Administration (FDA)

 Although these analyses arrived at fairly consistent conclusions, 

 is still only an approximation. The relative rankings apply within each class, but some classes as a whole are more sedating than others, particularly the antipsychotics.

Surprisingly, the traditional mood stabilizers, particularly lithium, are not nearly as sedating as the antipsychotics. Lithium has been reported to cause sedation in about 1 in 16 to 1 in 27 patients, depending on the study. With most second-generation antipsychotics, this rate is 

 While lithium may not cause much drowsiness, it does cause adverse effects that can be mistaken for sedation, like motoric and cognitive slowing, especially in higher concentrations.

There are 2 nonsedating antidepressants that have stimulant-like properties: bupropion and tranylcypromine. Tranylcypromine is a monoamine oxidase inhibitor (MAOI), but it is structurally related to amphetamine and has dopaminergic effects in the brain. Both of these medications are best dosed in the morning. However, their stimulating effects do not necessarily mean that they will disrupt sleep quality, as we will see later in this review. 

 shows the most and least sedating antidepressants within each class.

Sedation is rarely encountered when treating 

 (ADHD) with traditional stimulants, but it can be a problem with the nonstimulant treatment options. Sedation is a well-known side effect of the α2 agonists, particularly clonidine, but new data suggests that atomoxetine may also carry a high risk. In clinical trials of atomoxetine, only 1 in 20 patients reported fatigue.

 However, in the FDA postmarketing reporting system, atomoxetine ranked second for its propensity to prompt reports of somnolence. (The study ranked atomoxetine against 30 antidepressants since it has an antidepressant structure).

 If fatigue was rare in clinical trials of atomoxetine, why did it prompt so many reports of somnolence? The best explanation for this discrepancy is that peak plasma levels of atomoxetine can be 10-fold higher in CYP2D6 poor metabolizers. Therefore, while fatigue may be rare with this drug, it is likely to be quite severe in patients that do experience it.

When it comes to antipsychotics, finding a nonsedating option is like navigating between the fabled 

. Patients tend to experience akathisia when we select the less sedating options like lurasidone, risperidone, cariprazine, and aripiprazole. The more sedating ones, such as clozapine, olanzapine, quetiapine, and ziprasidone, are less likely to cause 

. When patients cannot tolerate either of these side effects, brexpiprazole and iloperidone are good options, with number needed to harm (NNH) above 30 for both sedation and akathisia.

 Lumateperone is also relatively free of akathisia, and its sedative effects are usually manageable with evening dosing.

Some medications are so sedating that this adverse effect limits their use. This is particularly true when they are taken in the morning, as is often the case for the short half-life medications that are given in divided doses. Quetiapine (half-life, 6 hours), ziprasidone (7 hours), clozapine (12 hours), and trazodone (5 to 9 hours) were all recommended for twice daily dosing when they were first released, based on the half-lives of the drugs. However, pragmatic physicians soon began dosing these medications at night without any loss of efficacy. This strategy is supported by about a dozen clinical trials comparing evening dosing to divided dosing in patients with schizophrenia and mood disorders.

 Asenapine could also be added to that list, as it was originally recommended to be given in divided doses but has a 24-hour half-life.

Sedation can be an asset when these short half-life medications are given at night, as their sedative effects are generally limited to the hours of sleep. The major risk with this strategy is orthostasis, particularly in older patients. For quetiapine, the extended-release version reduces this risk by smoothing over the peak levels.

When switching medications is not an option and evening dosing does not relieve sedation, antidotes may help, but are not consistently helpful. Modafinil and armodafinil improved residual fatigue in both bipolar and unipolar depression, but the benefit was small (effect size = 0.15).

 to improve fatigue in studies of patients with schizophrenia, although those trials were probably underpowered to detect the difference.

 Traditional stimulants have even less evidence of benefit and carry more risks. Concerns about tolerance, addiction, psychosis, mania, and cardiovascular risks significantly limit their use.

Psychiatric medications may cause fatigue through direct sedative effects or by worsening sleep quality. When medications make it difficult for a patient to fall asleep, the effect is usually readily apparent to the patient. When they disrupt sleep quality, the cause is less apparent. Poor sleep quality causes a variety of problems, some of which can be mistaken for symptoms of psychiatric disorders (eg, daytime fatigue, trouble concentrating, irritability, slowed reaction time, and poor problem-solving abilities).

Serotonergic antidepressants can cause both initiation insomnia and restless, fragmented sleep.

 The sedative effects of these antidepressants generally parallel their tendency to disrupt sleep, suggesting that poor sleep quality may be part of the reason that patients feel tired on these medications.

On the other hand, some antidepressants (eg, bupropion, levomilnacipran, and vortioxetine) have low rates of both sedation and insomnia.

 Despite its stimulating effects, bupropion actually improves sleep quality, increasing slow-wave sleep and reducing REM 

 Bupropion can cause difficulty falling asleep, but it does so at about the same rate as the selective serotonin reuptake inhibitors (SSRIs).

 Vortioxetine has not been adequately tested in a sleep lab, but it was 

 to normalize sleep architecture in an animal study and, in a post hoc analysis of a clinical study, it improved subjective reports of sleep quality.

If a patient needs a sedative to fall asleep, mirtazapine and trazodone both achieve this effect without worsening sleep quality. These antidepressants increase the slow waves that characterize the deepest stage of sleep.

 Likewise, the sedating antipsychotics usually do not worsen sleep quality, and may, in fact, improve it (

Quetiapine improved sleep quality, increased sleep efficiency, and reduced nocturnal awakenings in patients with bipolar disorder. Olanzapine, risperidone, and ziprasidone also resulted in improvements in sleep quality, beyond their effects on sleep initiation.19 Lumateperone, which shares a serotonin 5-HT2A receptor antagonist effect with trazodone, was originally developed as a hypnotic before gaining approval in schizophrenia. Taken nightly, in low doses (1-10 mg hs), lumateperone improved sleep without causing next-day sedation.

 These sedating options may provide dual benefits when patients require an antipsychotic for schizophrenia or a mood disorder, but antipsychotics have too many risks to justify their use for insomnia alone.

Sedation may not always be desirable, but it is difficult to avoid in psychiatry. Some of the most sedating medications have unique benefits that may justify their use (

 Evening dosing may improve tolerability, as long as adverse effects that are linked to the peak serum level do not get in the way. Orthostasis, for example, can cause a problem when antipsychotics and some antidepressants (eg, trazodone, mirtazapine, tricyclics, MAOIs) reach peak levels.

On the other hand, it is not necessary to jump to a sedating medication just because a patient has trouble sleeping. Some of these medications, like the SSRIs and the serotonin-norepinephrine reuptake inhibitors, worsen sleep quality. In fact, sleep may improve with an activating medication, either because it deepens sleep quality as bupropion does, or because it helps the patient reset their circadian rhythm. Patients tend to sleep better when they rise at regular times and stay active during the day.

is an instructor in clinical psychiatry at the Wake Forest School of Medicine and the director of the Mood Treatment Center in Winston-Salem, North Carolina. He is editor-in-chief of 

and coeditor of the Bipolar Disorder Section for 

Sedation, an unpleasant, undesirable and potentially dangerous side-effect of many psychotropic drugs.

 Hum Psychopharmacol. 2004;19(2):135-139.

2. Yun L, Fagan M, Subramaniapillai M, et al. 

Are early increases in physical activity a behavioral marker for successful antidepressant treatment?

Managing the Side Effects of Psychotropic Medications. 

2nd ed. American Psychiatric Association Publishing; 2019.

4. Citrome L. Activating and sedating adverse effects of second-generation antipsychotics in the treatment of schizophrenia and major depressive disorder: absolute risk increase and number needed to harm. 

5. Alberti S, Chiesa A, Andrisano C, Serretti A.

 Insomnia and somnolence associated with second-generation antidepressants during the treatment of major depression: a meta-analysis

Handbook of Diagnosis and Treatment of Bipolar Disorders. 

Acceptability of acute and maintenance pharmacotherapy of bipolar disorder: a systematic review of randomized, double-blind, placebo-controlled clinical trials

8. Cheng JY, Chen RY, Ko JS, Ng EM. Efficacy and safety of atomoxetine for attention-deficit/hyperactivity disorder in children and adolescents-meta-analysis and meta-regression analysis. 

9. Eugene AR. Association of sleep among 30 antidepressants: a population-wide adverse drug reaction study, 2004-2019. 

10. Takeuchi H, Powell V, Geisler S, et al. Clozapine administration in clinical practice: once-daily versus divided dosing. 

11. Chengappa KN, Parepally H, Brar JS, et al. A random-assignment, double-blind, clinical trial of once- vs twice-daily administration of quetiapine fumarate in patients with schizophrenia or schizoaffective disorder: a pilot study. 

12. Raatjes B, Dantz B. Trazodone: the forgotten antidepressant. 

13. Riesenberg RA, Baldytcheva I, Datto C. Self-reported sedation profile of quetiapine extended-release and quetiapine immediate-release during 6-day initial dose escalation in bipolar depression: a multicenter, randomized, double-blind, phase IV study. 

14. Goss AJ, Kaser M, Costafreda SG, et al. Modafinil augmentation therapy in unipolar and bipolar depression: a systematic review and meta-analysis of randomized controlled trials. 

15. Saavedra-Velez C, Yusim A, Anbarasan D, Lindenmayer JP. 

Modafinil as an adjunctive treatment of sedation, negative symptoms, and cognition in schizophrenia: a critical review

16. Alberti S, Chiesa A, Andrisano C, Serretti A. 

Insomnia and somnolence associated with second-generation antidepressants during the treatment of major depression: a meta-analysis

17. Ott GE, Rao U, Lin KM, et al. Effect of treatment with bupropion on EEG sleep: relationship to antidepressant response. 

18. Liguori C, Ferini-Strambi L, Izzi F, et al. 

Preliminary evidence that vortioxetine may improve sleep quality in depressed patients with insomnia: a retrospective questionnaire analysis

19. Monti JM. The effect of second-generation antipsychotic drugs on sleep parameters in patients with unipolar or bipolar disorder. 

20. Calsolaro V, Antognoli R, Okoye C, Monzani F. The use of antipsychotic drugs for treating behavioral symptoms in Alzheimer’s disease. 

Schatzberg’s Manual of Clinical Psychopharmacology.

 9th ed. American Psychiatric Association Publishing; 2019.❒

Sedation may not always be desirable, but it is difficult to avoid in psychiatry. Some of the most sedating medications are discussed.

Sedation: The Ups and Downs of a Side Effect

Between mid-February and mid-March 2020, the number of sleep prescriptions in the United States rose by 14.8%. The increase may be due to the pandemic, says Manoj Malhotra, MD. Based on his experience, he says “the current environment, with myriads of shifts in our day-to-day lives, is a perfect storm for sleep challenges.”

In this Mental Health Minute, Malhotra explains how to distinguish between a general lack of sleep and chronic insomnia, and how to treat the latter.

 is vice president, United States medical affairs for the neurology business group at Eisai.

Have you seen more patients with sleep problems during the pandemic? 

Share comments with your colleagues by emailing 

. Comments may be shared online pending review and editing for style.

Key considerations for healthcare providers seeking to manage their patients’ insomnia.  

The COVID-19 Pandemic Is a Perfect Storm for Sleep Challenges

The US Food and Drug Administration (FDA) recently accepted the new drug application (NDA) for Idorsia’s investigational dual orexin receptor antagonist, daridorexant, designed for the treatment of 

“I’m very happy that this first regulatory hurdle is behind us,” said Jean-Paul Clozel, MD, Chief Executive Officer of Idorsia. “This was a huge NDA and the team has done an excellent job in preparing the dossier, on which the FDA can judge the properties and merits of daridorexant. We now stand-by to work with the FDA to answer any questions that might arise concerning the effect of daridorexant on sleep, daytime functioning, and its safety profile.”

Daridorexant targets overactive wakefulness associated with insomnia by blocking the activity of orexin, has a rapid onset, and lasts long enough to cover the night without any next-morning residual sleepiness. According to data from the phase 3 registration program, daridorexant is the first insomnia treatment to show statistically significant and clinically meaningful improvements in daytime functioning, sustained over time, as well as sleep during the night.

“While we designed daridorexant to have the optimal profile for a sleep medicine, I am none-the-less stunned by the results. Once approved, by providing daridorexant to the millions of patients with insomnia, Idorsia will have a major impact on this medical, social, and economic problem,” Clozel said. “It has struck me particularly in these times of confinement that we are living through, that sleep problems are a major issue and require an extremely safe and effective drug that can be used by the many. With these results Idorsia is entering into a new era; less than 3 years since its creation, Idorsia is taking a huge step forward in delivering on the vision to become a fully-fledged biopharmaceutical company.”

Adverse events included headache, somnolence, fatigue, dizziness, and nausea, although the incidence of somnolence was low and did not increase with daridorexant 50 mg when compared with placebo.

Idorsia submitted the NDA on January 8, 2021 and anticipates a US launch in the first half of 2022, should approval be received.

1. Idorsia Pharmaceuticals. FDA accepts the new drug application for review of Idorsia’s daridorexant for the treatment of adult patients with insomnia. 

https://www.globenewswire.com/news-release/2021/03/10/2190042/0/de/FDA-accepts-the-new-drug-application-for-review-of-Idorsia-s-daridorexant-for-the-treatment-of-adult-patients-with-insomnia.html

2. Idorsia Pharmaceuticals. Idorsia announces positive results in the first Phase 3 study of daridorexant with improved overall sleep and daytime performance of patients with insomnia. News release. April 20, 2020. 

https://www.idorsia.com/media/news-details?newsId=2284972

This investigational dual orexin receptor antagonist improved sleep overnight and daytime functioning. 

Insomnia Treatment Without Daytime Sleepiness

Teralyn Sell, PhD, MS, NCC, LPC, provides tips on what late night snacks could disrupt sleep patterns. 

Blueberries Treat Depression, With a Catch

holds a doctorate in psychology and is the founder of Pro Recovery Rx, a supplement line dedicated to supporting brain health for individuals in addiction recovery. She also teaches a class called NeuroHealth Coach, which helps professionals integrate brain health into their daily lives.

The key to better sleep? Stabilizing blood sugar. 

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Nightmare disorder can produce emotional manifestations of fear, anger, and sadness. Here are 7 reasons parasomnias can challenge even the most astute diagnostician.

7 Things to Know About Parasomnias

The US Food and Drug Administration (FDA) has accepted Avadel Pharmaceuticals New Drug Application (NDA) for FT218 for review. FT218 is a formulation of sodium oxybate that uses Avadel’s MicroPump™ controlled-release (CR) technology for the treatment of severe daytime sleepiness and cataplexy in adults with narcolepsy.

“The FDA’s acceptance of our NDA for once-nightly FT218 and assignment of a PDUFA target action date of October 15th represents another important milestone on the path towards receiving approval. We are confident in our regulatory filing strategy and we look forward to working with the Agency in our pursuit of bringing this important treatment to patients,” Greg Divis, Chief Executive Officer of Avadel, said to the press. “If approved, FT218 will be the first and only once-nightly oxybate medication, a significant advancement to the twice-nightly regimen that has been required for nearly 20 years.”

Avadel’s NDA submission is supported by positive data from the phase 3 REST-ON study, completed under a Special Protocol Assessment (SPA) agreement with the FDA. In the first half of 2021, Avadel intends to present data from the study for the 3 primary endpoints, a number of secondary endpoints, and post-hoc analyses at upcoming conferences.

“It’s important to remember that FT218 was granted Orphan Drug Designation by the FDA based on the plausible hypothesis that it may be clinically superior to the twice-nightly formulation of sodium oxybate already approved by the Agency for the same indication. If the FDA approves FT218 and grants Orphan Drug Exclusivity, then we would be awarded a seven-year period of market exclusivity in the US,” said Divis.

The FDA assigned the NDA a Prescription Drug User Fee Act (PDUFA) target action date of October 15, 2021.

Additionally, 4 phase studies from the FT218 pharmacokinetic program will be published in the article, “Pharmacokinetics of FT218, a Once-Nightly Sodium Oxybate Formulation in Healthy Adults,” in 

“These data should instill confidence in clinicians and patients regarding the robust phase 1 development program for FT218, with the demonstration of predictable blood levels of the active ingredient with a single dose, and a low residual amount of active drug remaining when a patient would awaken,” David Seiden, MD, lead author and senior medical director of clinical development and medical affairs at Avadel Pharmaceuticals, told the press. “As a sleep medicine physician and researcher, I am pleased that we have leveraged our proven technology to move toward the goal of patients potentially having access to a once-nightly sodium oxybate treatment.”

1. Avadel Pharmaceuticals. Avadel Pharmaceuticals announces FDA acceptance of New Drug Application for FT218 in adults with narcolepsy for the treatment of excessive daytime sleepiness and cataplexy. News release. March 1, 2021. 

https://www.globenewswire.com/news-release/2021/03/01/2184208/0/en/Avadel-Pharmaceuticals-Announces-FDA-Acceptance-of-New-Drug-Application-for-FT218-in-Adults-with-Narcolepsy-for-the-Treatment-of-Excessive-Daytime-Sleepiness-and-Cataplexy.html

2. Avadel Pharmaceuticals. Avadel Pharmaceuticals announces publication of once-nightly FT218 pharmacokinetic studies. News release. March 2, 2021. 

https://investors.avadel.com/news-releases/news-release-details/avadel-pharmaceuticals-announces-publication-once-nightly-ft218

If approved, this formulation of sodium oxybate will be the first once-nightly oxybate treatment for daytime sleepiness. 

Sleepiness Treatment Under FDA Review 

Thomas So, PharmD, discusses getting a better night's sleep, even during the pandemic. 

is Manager at the Meducation Group at First Databank (FDB). 

The stress and anxiety of the COVID-19 pandemic might be interfering with sleep patterns. 

Coronasomnia

Andrew Krystal, MD, discusses his recent publication, 

Cost-effectiveness of digital CBT (Sleepio) for insomnia: A Markov simulation model in the United States

is a psychiatrist who cares for adults with all types of sleep disorders, with particular expertise in insomnia. He also treats patients who have mood and anxiety spectrum disorders in addition to sleep disorders. An internationally renowned expert on sleep and mood disorders, he has more than 25 years of experience in patient care and research. He is president of the Sleep Research Society and a member of the American Academy of Sleep Medicine, American Psychiatric Association and American College of Neuropsychopharmacology. He serves on the examination committee of the American Board of Sleep Medicine, which allows medical professionals to pursue certification in sleep medicine.

How cost-effective is fully automated digital cognitive behavioral therapy (CBT) intervention for insomnia?

Digital Cognitive Behavior Therapy for Insomnia 

At the recent Virtual SLEEP 2020 Meeting, Eisai gave 2 presentations. One of these was on lemborexant, which was recently launched in the US for the treatment of adult patients with insomnia, characterized by difficulties with sleep onset and/or sleep maintenance.

In these presentations, data on the following topics were shared:

1. Long-term results evaluating lemborexant efficacy and safety in adults ages 65 and older, in measures of time to sleep onset, sleep efficacy, and sleep maintenance.

2. Efficacy and safety results of lemborexant in female subjects of perimenopausal age from SUNRISE 2.

3. An open-label pilot study evaluating the ability of patients with insomnia disorder to directly transition from zolpidem to lemborexant. 

4. The impact of lemborexant on fatigue severity.

is the International Project Team Lead for the lemborexant clinical development program at Eisai. 

The International Project Team Lead for the lemborexant clinical development program shares insights from their presentations at the Virtual SLEEP 2020 Meeting. 

Sleep Disorders